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Relevant bibliographies by topics / Kidney cells

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Academic literature on the topic 'Kidney cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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Journal articles on the topic "Kidney cells"

1

Yokote, Shinya, Shuichiro Yamanaka, and Takashi Yokoo. "De NovoKidney Regeneration with Stem Cells." Journal of Biomedicine and Biotechnology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/453519.

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Recent studies have reported on techniques to mobilize and activate endogenous stem-cells in injured kidneys or to introduce exogenous stem cells for tissue repair. Despite many recent advantages in renal regenerative therapy, chronic kidney disease (CKD) remains a major cause of morbidity and mortality and the number of CKD patients has been increasing. When the sophisticated structure of the kidneys is totally disrupted by end stage renal disease (ESRD), traditional stem cell-based therapy is unable to completely regenerate the damaged tissue. This suggests that whole organ regeneration may be a promising therapeutic approach to alleviate patients with uncured CKD. We summarize here the potential of stem-cell-based therapy for injured tissue repair andde novowhole kidney regeneration. In addition, we describe the hurdles that must be overcome and possible applications of this approach in kidney regeneration.

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Law, Becker M. P., Ray Wilkinson, Xiangju Wang, Katrina Kildey, Kurt Giuliani, Kenneth W. Beagley, Jacobus Ungerer, Helen Healy, and Andrew J. Kassianos. "Human Tissue-Resident Mucosal-Associated Invariant T (MAIT) Cells in Renal Fibrosis and CKD." Journal of the American Society of Nephrology 30, no. 7 (June 11, 2019): 1322–35. http://dx.doi.org/10.1681/asn.2018101064.

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BackgroundMucosal-associated invariant T (MAIT) cells represent a specialized lymphocyte population associated with chronic inflammatory disorders. Little is known, however, about MAIT cells in diseases of the kidney, including CKD.MethodsTo evaluate MAIT cells in human native kidneys with tubulointerstitial fibrosis, the hallmark of CKD, we used multicolor flow cytometry to identify, enumerate, and phenotype such cells from human kidney tissue biopsy samples, and immunofluorescence microscopy to localize these cells. We cocultured MAIT cells and human primary proximal tubular epithelial cells (PTECs) under hypoxic (1% oxygen) conditions to enable examination of mechanistic tubulointerstitial interactions.ResultsWe identified MAIT cells (CD3+ TCR Vα7.2+ CD161hi) in healthy and diseased kidney tissues, detecting expression of tissue-resident markers (CD103/CD69) on MAIT cells in both states. Tissue samples from kidneys with tubulointerstitial fibrosis had significantly elevated numbers of MAIT cells compared with either nonfibrotic samples from diseased kidneys or tissue samples from healthy kidneys. Furthermore, CD69 expression levels, also an established marker of lymphocyte activation, were significantly increased on MAIT cells from fibrotic tissue samples. Immunofluorescent analyses of fibrotic kidney tissue identified MAIT cells accumulating adjacent to PTECs. Notably, MAIT cells activated in the presence of human PTECs under hypoxic conditions (modeling the fibrotic microenvironment) displayed significantly upregulated expression of CD69 and cytotoxic molecules perforin and granzyme B; we also observed a corresponding significant increase in PTEC necrosis in these cocultures.ConclusionsOur findings indicate that human tissue-resident MAIT cells in the kidney may contribute to the fibrotic process of CKD via complex interactions with PTECs.

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Valiño-Rivas, Lara, Leticia Cuarental, Mateo Agustin, Holger Husi, Pablo Cannata-Ortiz, Ana B. Sanz, Harald Mischak, Alberto Ortiz, and Maria Dolores Sanchez-Niño. "MAGE genes in the kidney: identification of MAGED2 as upregulated during kidney injury and in stressed tubular cells." Nephrology Dialysis Transplantation 34, no. 9 (December 11, 2018): 1498–507. http://dx.doi.org/10.1093/ndt/gfy367.

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Abstract Background Mutations in Melanoma Antigen-encoding Gene D2 (MAGED2) promote tubular dysfunction, suggesting that MAGE proteins may play a role in kidney pathophysiology. We have characterized the expression and regulation of MAGE genes in normal kidneys and during kidney disease. Methods The expression of MAGE genes and their encoded proteins was explored by systems biology multi-omics (kidney transcriptomics and proteomics) in healthy adult murine kidneys and following induction of experimental acute kidney injury (AKI) by a folic acid overdose. Changes in kidney expression during nephrotoxic AKI were validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blot and immunohistochemistry. Factors regulating gene expression were studied in cultured tubular cells. Results Five MAGE genes (MAGED1, MAGED2, MAGED3, MAGEH1, MAGEE1) were expressed at the mRNA level in healthy adult mouse kidneys, as assessed by RNA-Seq. Additionally, MAGED2 was significantly upregulated during experimental AKI as assessed by array transcriptomics. Kidney proteomics also identified MAGED2 as upregulated during AKI. The increased kidney expression of MAGED2 mRNA and protein was confirmed by qRT-PCR and western blot, respectively, in murine folic acid- and cisplatin-induced AKI. Immunohistochemistry located MAGED2 to tubular cells in experimental and human kidney injury. Tubular cell stressors [serum deprivation and the inflammatory cytokine tumour necrosis factor-like weak inducer of apoptosis (TWEAK)] upregulated MAGED2 in cultured tubular cells. Conclusions MAGED2 is upregulated in tubular cells in experimental and human kidney injury and is increased by stressors in cultured tubular cells. This points to a role of MAGED2 in tubular cell injury during kidney disease that should be dissected by carefully designed functional approaches.

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Baban, Babak, Jun Yao Liu, and Mahmood S. Mozaffari. "Aryl hydrocarbon receptor agonist, leflunomide, protects the ischemic-reperfused kidney: role of Tregs and stem cells." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 11 (December 1, 2012): R1136—R1146. http://dx.doi.org/10.1152/ajpregu.00315.2012.

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The aryl hydrocarbon receptor (AHR) has emerged as a major modulator of inflammatory processes. We tested the hypothesis that AHR activation protects the ischemic-reperfused kidney in association with the suppression of the inflammatory response. Accordingly, male mice were treated with the nondioxin AHR agonist, leflunomide (40 mg/kg ip); vehicle-treated animals served as controls. Thereafter, the right kidney was subjected to an ischemia (45 min)-reperfusion (4 h) insult, while the left kidney served as a sham control. Renal cells prepared from ischemic-reperfused kidneys of leflunomide-treated mice displayed preservation of mitochondrial membrane potential (Ψm) and decreased apoptosis and necrosis compared with vehicle-treated ischemic-reperfused kidneys. Leflunomide treatment increased regulatory T cells (Tregs; forkhead box P3+) and IL-10-positive cells but reduced IL-17- and IL-23-expressing cells in both the peripheral blood and kidney cells, indicative of down-regulation of inflammatory responses. Leflunomide treatment also increased mobilization of stems cells subsets (i.e., mesenchymal and hematopoietic stem cells and endothelial progenitor cells) in the peripheral blood and promoted their recruitment into the ischemic-reperfused kidney. Collectively, the results indicate that AHR stimulation may represent a novel renoprotective mechanism likely involving mobilization and recruitment of Tregs and stem cells into the damaged kidney.

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Kim, Bo Hye, Do Yeon Kim, Yejin Ahn, Eun Ji Lee, Hyunjoo Park, Meeyoung Park, and Jong Hoon Park. "Semaphorin-3C Is Upregulated in Polycystic Kidney Epithelial Cells and Inhibits Angiogenesis of Glomerular Endothelial Cells." American Journal of Nephrology 51, no. 7 (2020): 556–64. http://dx.doi.org/10.1159/000508263.

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Background: Polycystic kidney disease (PKD) is a hereditary disease characterized by cyst formation in the kidneys bilaterally. It has been observed that semaphorin-3C (SEMA3C) is overexpressed in polycystic kidney epithelial cells. It is hypothesized that upregulated SEMA3C would contribute to survival of polycystic kidney epithelial cells. Furthermore, as the kidney is a highly vascularized organ, the secreted SEMA3C from PKD epithelial cells will affect glomerular endothelial cells (GECs) in a paracrine manner. Methods: To evaluate the effect of SEMA3C on renal cells, siSEMA3C-treated PKD epithelial cells were used for further analysis, and GECs were exposed to recombinant SEMA3C (rSEMA3C). Also, co-culture and treatment of conditioned media were employed to confirm whether PKD epithelial cells could influence on GECs via SEMA3C secretion. Results: SEMA3C knockdown reduced proliferation of PKD epithelial cells. In case of GECs, exposure to rSEMA3C decreased angiogenesis, which resulted from suppressed migratory ability not cell proliferation. Conclusions: This study indicates that SEMA3C is the aggravating factor in PKD. Thus, it is proposed that targeting SEMA3C can be effective to mitigate PKD.

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Zhang, Zhu-Xu, Jifu Jiang, Xuyan Huang, Ziqin Yin, Weihua Liu, Bertha Garcia, and Anthony Jevnikar. "NK cells mediate chronic kidney allograft injury (169.26)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 169.26. http://dx.doi.org/10.4049/jimmunol.186.supp.169.26.

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Abstract Chronic allograft injury remains the leading cause of kidney graft loss after transplantation and no-specific therapy currently exist. We have recently demonstrated that NK cells can kill syngeneic tubular epithelial cells (TEC) and participate in kidney ischemia-reperfusion injury. In this study, we investigated the capacity of NK cells to mediate kidney injury in transplantion. C57BL/6 (B6, H-2b) kidneys were transplanted into nephrectomized F1 (B6 x BALB/c, CB6F1) mice. Serum creatinine levels increased from baseline (22+5 uM, n=8) to 38±6 uM (n=6, P<0.001) at 60 days post transplant, demonstrating a clear loss of kidney function. Infiltrates and low grade renal tubular cell injury were consistently present in B6-to-CB6F1transplants suggesting a non T cell pathway. This was supported by results using a B6-Rag-/--to- CB6F1Rag-/- (B6Rag-/-xBALB/cRag-/-) F1 kidney transplant that eliminates T and B cell but not NK cell participation. Similar levels of kidney dysfunction (creatinine: 34+8 uM, n=6, p<0.01) and histological injury were observed 65 days post transplant. Finally depletion of NK cells prevented kidney injury (25±6 vs 34+8 uM in no antibody injection, n=6, p<0.05) as well as improved histology. In conclusion, these data demonstrate for the first time a critical role for NK cells in mediating chronic kidney injury, which is independent of T and B cells. NK cells are newly appreciated and formidable effectors to chronic kidney injury and graft loss.

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Jang, Hee-Seong, Jee In Kim, Sang Jun Han, and Kwon Moo Park. "Recruitment and subsequent proliferation of bone marrow-derived cells in the postischemic kidney are important to the progression of fibrosis." American Journal of Physiology-Renal Physiology 306, no. 12 (June 15, 2014): F1451—F1461. http://dx.doi.org/10.1152/ajprenal.00017.2014.

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Acute kidney injury (AKI) is an independent risk factor of the development of chronic kidney disease. Kidney fibrosis is a typical feature of chronic kidney disease and is characterized as an expansion of the interstitium due to increases in extracellular matrix molecules and interstitial cells caused by accumulations of extrarenal cells and by the proliferation or differentiation of intrarenal cells. However, the role of bone marrow-derived cells (BMDCs) in AKI-induced kidney fibrosis remains to be defined. Here, we investigated the role of BMDCs in kidney fibrosis after ischemia-reperfusion injury (IRI)-induced AKI in green fluorescent protein (GFP)-expressing bone marrow chimeric mice. IRI resulted in severe fibrotic changes in kidney tissues and dramatically increased interstitial cell numbers. Furthermore, GFP-expressing BMDCs accounted for >80% of interstitial cells in fibrotic kidneys. Interstitial GFP-expressing cells expressed α-smooth muscle actin (a myofibroblast marker), fibroblast-specific protein-1 (a fibroblast marker), collagen type III, and F4/80 (a macrophage marker). Over 20% of interstitial cells were bromodeoxyuridine-incorporating (proliferating) cells, and of these, 80% cells were GFP-expressing BMDCs. Daily treatment of IRI mice with apocynin (a NADPH oxidase inhibitor that functions as an antioxidant) from the day after surgery until euthanization slightly inhibited these changes with a small reduction of fibrosis. Taken together, our findings show that BMDCs make a major contribution to IRI-induced fibrosis due to their infiltration, subsequent differentiation, and proliferation in injured kidneys, suggesting that BMDCs be considered an important target for the treatment of kidney fibrosis.

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Du, Ao-Ling, Dan Liu, Wen-Hui Zhang, and Sheng-Hua Chen. "The Development of Endothelial Cells in Revascularization of Blood Vessels in Kidney Scaffolds." Journal of Biomaterials and Tissue Engineering 9, no. 9 (September 1, 2019): 1167–78. http://dx.doi.org/10.1166/jbt.2019.2122.

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The kidney is an important organ of the human body. However, the morbidity and mortality of endstage renal disease (ESRD) have been increasing year after year. Currently, the best treatment for ESRD is kidney transplantation. However, the extreme lack of donor kidneys causes many people to die in queues waiting for a kidney source. Fortunately, recent advances in bioengineering, stem cells, and regenerative medicine have raised new hopes that there may be a viable way to form new transplantable kidneys. Kidney scaffolds have had all cellular components removed, but retain intact extracellular matrix (ECM). However, there are still many challenges, such as thrombosis, before this potential therapy can be used in clinical patients. Vascularization is a key part of the success of tissue engineering and a vital factor for maintaining organ function. Endothelial cells are crucial in the formation of vessels in kidney scaffolds. The primary challenge of recellularized kidney scaffolds is to re-endothelialize the renal vasculature. Unfortunately, until now, there have been no report demonstrating successful vascularization in bioengineering kidney scaffolds, such as uniform endothelial cell coverage of vascular walls, no thrombosis and blood flow maintenance for a long time. Hence, this review mainly discusses the development of endothelial cells in the re-endothelialized vasculature of renal scaffolds.

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Salcido-Ochoa, Francisco, Susan Swee-Shan Hue, Doreen Haase, Jason Chon Jun Choo, Nurhashikin Yusof, Reiko Lixiang Li, John Carson Allen, Jabed Iqbal, Alwin Hwai Liang Loh, and Olaf Rotzschke. "Analysis of T Cell Subsets in Adult Primary/Idiopathic Minimal Change Disease: A Pilot Study." International Journal of Nephrology 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/3095425.

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Aim. To characterise infiltrating T cells in kidneys and circulating lymphocyte subsets of adult patients with primary/idiopathic minimal change disease. Methods. In a cohort of 9 adult patients with primary/idiopathic minimal change recruited consecutively at disease onset, we characterized (1) infiltrating immune cells in the kidneys using immunohistochemistry and (2) circulating lymphocyte subsets using flow cytometry. As an exploratory analysis, association of the numbers and percentages of both kidney-infiltrating immune cells and the circulating lymphocyte subsets with kidney outcomes including deterioration of kidney function and proteinuria, as well as time to complete clinical remission up to 48 months of follow-up, was investigated. Results. In the recruited patients with primary/idiopathic minimal change disease, we observed (a) a dominance of infiltrating T helper 17 cells and cytotoxic cells, comprising cytotoxic T cells and natural killer cells, over Foxp3+ Treg cells in the renal interstitium; (b) an increase in the circulating total CD8+ T cells in peripheral blood; and (c) an association of some of these parameters with kidney function and proteinuria. Conclusions. In primary/idiopathic minimal change disease, a relative numerical dominance of effector over regulatory T cells can be observed in kidney tissue and peripheral blood. However, larger confirmatory studies are necessary.

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Ko, Gang Jee, Douglas Linfert, Hye Ryoun Jang, Elizabeth Higbee, Tonya Watkins, Chris Cheadle, Manchang Liu, Lorraine Racusen, Dmitry N. Grigoryev, and Hamid Rabb. "Transcriptional analysis of infiltrating T cells in kidney ischemia-reperfusion injury reveals a pathophysiological role for CCR5." American Journal of Physiology-Renal Physiology 302, no. 6 (March 15, 2012): F762—F773. http://dx.doi.org/10.1152/ajprenal.00335.2011.

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Although T cells have been shown to play a direct role in kidney ischemia-reperfusion injury (IRI), little is known about the underlying mechanisms. We hypothesized that studying the transcriptional responses in kidney-infiltrating T cells would help elucidate novel therapeutic targets for kidney IRI. Unilateral renal pedicle clamping for 45 min was performed in male C57BL/6 mice, and CD3+ T cells were isolated from the kidney and purified. Transcriptional activities of T cell were measured by array-based PCR compared between ischemic kidneys and contralateral nonischemic kidneys. Among total of 89 genes analyzed, 24, 22, 24, and 37 genes were significantly changed at 6 h, day 3, day 10, and day 28 after IRI. Genes associated with cytokines, chemokines, and costimulatory molecules were upregulated. Pathway analysis identified CC motif chemokine receptor 5 (CCR5) as a candidate pathophysiological pathway. CCR5 upregulation was validated at the protein level, and CCR5 blockade improved renal function after kidney IRI. Using discovery techniques to identify transcriptional responses in purified kidney-infiltrating cells enabled the elucidation of novel mechanisms and therapeutic targets for IRI.

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Dissertations / Theses on the topic "Kidney cells"

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Tang, Chi-wai Sydney. "The many facets of the renal proximal tubular epithelial cell in human." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B31992468.

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Tang, Chi-wai Sydney, and 鄧智偉. "The many facets of the renal proximal tubular epithelial cell inhuman." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B31992468.

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Chen, Titi. "Type 1 conventional dendritic cells in kidney disease." Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/27814.

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Dendritic cells (DCs) are central orchestrators of the immune system, which regulate both innate and adaptive immune responses. They can be broadly categorized into plasmacytoid DCs (pDCs) and conventional DCs (cDCs). cDC1s are a major subset of conventional DCs and play an important role in kidney disease. In this study, I firstly examined cDC1s in human kidney disease through analysing frozen human kidney biopsy samples. Secondly, I investigated the mechanisms of effects of cDC1s in experimental kidney disease, namely Adriamycin nephropathy and anti-GBM disease. Lastly, I explored the therapeutic potential of targeting cDC1s by repurposing Flt3 inhibitor for treatment of kidney disease. In the human study, I found that the number of cDC1s correlated with disease severity in acute tubular necrosis, number of crescents in pauci-immune glomerular nephritis, interstitial fibrosis in IgA nephropathy and lupus nephritis, as well as prognosis in IgA nephropathy. The number of CD8+ T cells also increased significantly in these conditions and cDC1 number correlated with CD8+ T cell number. These findings reflected a possible role of cDC1s in these conditions and their association with CD8+ T cells suggested a combined mechanism in keeping with the results in animal models. In the animal experiments, I studied cDC1s in vitro and in vivo using wild type as well as transgenic XCR1-DTR mice. In both Adriamycin nephropathy and anti-GBM disease, I found the number of cDC1s increased significantly. Depletion of cDC1s attenuated kidney injury, suggesting their pathogenic role. The mechanisms underlying cDC1 mediated kidney injury was demonstrated to relate to their superior ability to activate CD8+ T cells. Flt3 is a receptor tyrosine kinase which regulates the differentiation of DCs and a Flt3 inhibitor is currently being used in cancer treatment. I demonstrated that a Flt3 inhibitor can deplete cDC1s with relative specificity. The Flt3 inhibitor attenuated kidney injury in both Adriamycin nephropathy and anti-GBM disease. Therefore, repurposing Flt3 inhibitor could be a novel therapeutic strategy to treat kidney disease.

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Mora, Cristina Fuente. "Isolation and characterization of a novel population of potential kidney stem cells from postnatal mouse kidney." Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.507193.

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Brunskill, Nigel John. "Binding and uptake of albumin by opossum kidney cells." Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29459.

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Assays of both fluid phase endocytosis and receptor mediated endocytosis have been developed in opossum kidney cells. The regulation of the endocytic pathway has been examined using a number of potential inhibitors. In particular, bacterial toxins have been employed to identify potential points of regulation of the pathway by GTP-binding proteins. The apical endocytic pathway in these cells has been examined morphologically using electron microscopy of gold-albumin.;Based on the results of the above experiments a rat cDNA encoding the G-protein subunit G13 has been subcloned into pcDNA3. This vector has been stably transfected into opossum kidney cells by the calcium phosphate method. Over-expressing transfects have been selected and screened by western blotting and immunocytochemistry. These stable transfects have been used to measure albumin endocytosis and the results compared to control transfects and wild type cells.;Two binding sites for albumin have been identified, each with a different affinity. Based on the lectin competition studies the receptors appear to be glycoproteins carrying O-linked sugars. Specificity experiments indicate that the receptors share many similar characteristics to the family of scavenger receptors. [125I]-albumin ligand blotting has revealed the presence of three specific albumin binding proteins.;Endocytosis has been visualised using electron microscopy, with gold- albumin being seen in multiple intracellular vesicular structures. These endocytic pathways can be regulated by GTP-binding protein modulating agents. Opossum kidney cells have been successfully transfected with the Gi3 protein subunit. These cells show enhanced uptake of albumin compared to controls.;Therefore the experiments described in the thesis document the characteristics of albumin binding to opossum kidney cells, identify the potential receptors involved, and explore the mechanism of regulation of the subsequent endocytic uptake of albumin by the cells.

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Measures, H. R. "A study of desmosome formation in kidney epithelial cells." Thesis, University of Southampton, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234435.

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Lim, Ai Ing, and 林艾盈. "Shedding of kidney injury molecule-1 by kidney proximal tubular epithelial cells: the role of matrixmetalloproteinase-3." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49799745.

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Regardless of the original cause and etiology, the progression of kidney disease follows a final common pathway associated with tubulointerstitial injury, in which proximal tubular epithelial cells (PTEC) are instrumental. Kidney injury molecule-1 (KIM-1) is an emerging biomarker of kidney tubular damage. It is markedly expressed and released into urine in various animal models and human kidney diseases. This study aimed to explore the underlying mechanism regulating the release of KIM-1 by PTEC. First, expression and release of KIM-1 by primary cultured human PTEC were examined. In quiescent PTEC, KIM-1 was detected at the plasma membrane and in the cytoplasm. A transwell system, in which PTEC were grown as monolayer on permeable membrane, was used to examine the polarized release of KIM-1. PTEC constitutively released KIM-1 from their apical surface, and the release was independent of gene expression or protein synthesis. The KIM-1 release process by PTEC was enhanced dose- and time-dependently by two important kidney injury mediators, human serum albumin (HSA) and tumor necrosis factor (TNF)-α, and was inhibited by the presence of broad-spectrum inhibitors of matrix metalloproteinases (MMP). Second, the potential sheddases responsible for KIM-1 shedding were identified by quantitative polymerase chain reaction (PCR) array system, in which the gene expression of a panel of MMP members was screened. The gene expression of MMP-3, MMP-7 and MMP-9 was up-regulated by PTEC under HSA or TNF-α activation. Blockade experiments with synthetic MMP inhibitors or MMP gene knockdown by small interfering RNA transfection, revealed that the constitutive or accelerated KIM-1 shedding was mediated by MMP-3, but not MMP-7 or MMP-9. The role of MMP-3 in KIM-1 shedding was further defined by additional data showing the enhanced MMP-3 synthesis by HSA- or TNF-α-stimulated PTEC, and the up-regulated KIM-1 shedding by PTEC following exogenous MMP-3 treatment. Third, the regulatory mechanism of MMP-3-mediated KIM-1 shedding was investigated. Treatment of PTEC with HSA or TNF-α up-regulated the reactive oxygen species (ROS) generation, and its kinetics ran parallel to the increase of KIM-1 shedding and MMP-3 synthesis. In addition, exogenous hydrogen peroxide dose-dependently induced KIM-1 shedding and MMP-3 synthesis, which were abolished by the presence of an oxidation inhibitor. These evidence suggest that ROS play an essential role in regulating the MMP-3-mediated KIM-1 shedding by PTEC. Finally, a mouse model of acute kidney injury induced by renal ischemia and reperfusion (I/R) was established to translate the in vitro findings. Reduced kidney function and increased urinary KIM-1 level were observed in mice after renal I/R treatment. Strikingly, the expression of MMP-3 and KIM-1 in the I/R treated mice was most profound in the S3 segments of the proximal tubules, where is the most susceptible area to oxidative stress. Taken together, these in vivo data have further strengthened the distinct roles of ROS and MMP-3 in KIM-1 shedding during PTEC injury. In conclusion, ROS generated by the injured PTEC activate MMP-3, which release the soluble KIM-1 through the ectodomain shedding process.
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Medicine
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Sampangi, Sandeep. "Autologous human kidney proximal tubule epithelial cells (PTEC) modulate dendritic cell (DC), T cell and B cell responses." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/82033/1/Sandeep_Sampangi_Thesis.pdf.

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This is a comprehensive study of human kidney proximal tubular epithelial cells (PTEC) which are known to respond to and mediate the pathological process of a range of kidney diseases. It identifies various molecules expressed by PTEC and how these molecules participate in down-regulating the inflammatory process, thereby highlighting the clinical potential of these molecules to treat various kidney diseases. In the disease state, PTEC gain the ability to regulate the immune cell responses present within the interstitium. This down-regulation is a complex interaction of contact dependent/independent mechanisms involving various immuno-regulatory molecules including PD-L1, sHLA-G and IDO. The overall outcome of this down-regulation is suppressed DC maturation, decreased number of antibody producing B cells and low T cell responses. These manifestations within a clinical setting are expected to dampen the ongoing inflammation, preventing the damage caused to the kidney tissue.

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Prodromidi, Evangelia. "Contribution of bone marrow-derived stem cells to kidney regeneration." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444168.

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Katsoulieris, Elias. "Oxidatives and Endoplasmic Reticulum Stress in Kidney Priximal Tubule Cells." Thesis, University of Brighton, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506517.

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Books on the topic "Kidney cells"

1

Glomerulopathies: Cell biology and immunology. Australia: Harwood Academic Press, 1996.

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International, Meeting on Anion Transport Protein of the Red Blood Cell Membrane as well as Kidney and Diverse Cells (1989 Fukuoka-shi Japan). Anion transport protein of the red blood cell membrane: Proceedings of the International Meeting on Anion Transport Protein of the Red Blood Cell Membrane as well as Kidney and Diverse Cells, Fukuoka, 1-3 May 1989. Amsterdam: Elsevier, 1989.

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Edson, Pontes J., and Bukowski Ronald M, eds. Clinical management of renal cell cancer. Chicago: Year Book Medical Publishers, 1990.

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L, Minetti, D'Amico G. 1929-, and Ponticelli C, eds. The Kidney in plasma cell dyscrasias. Dordrecht: Kluwer Academic Publishers, 1988.

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Minetti, Luigi, Giuseppe D’Amico, and Claudio Ponticelli, eds. The Kidney in Plasma Cell Dyscrasias. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1315-8.

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Debruyne, F. M. J., 1941- and Ackermann R. 1941-, eds. Immunotherapy of renal cell carcinoma: Clinical and experimental developments. Berlin: Springer-Verlag, 1991.

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Lara, Primo N., and Eric Jonasch. Kidney cancer: Principles and practice. Heidelberg: Springer-Verlag, 2012.

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C, Bollack, Jacqmin D, and European Organization for Research on Treatment of Cancer. Genito-Urinary Tract Cancer Cooperative Group., eds. Basic research and treatment of renal cell carcinoma metastasis: Proceedings of an EORTC Genitourinary Group meeting, held in Strasbourg, France, November 4, 1988. New York: Wiley-Liss, 1990.

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Renal cell carcinoma. Shelton, Conn: People's Medical Pub. House, 2009.

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International Subcellular Methodology Forum (10th 1986 University of Surrey). Cells, membranes, and disease, including renal. New York: Plenum Press, 1987.

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Book chapters on the topic "Kidney cells"

1

Evan, A. P., and J. A. McAteer. "Cyst Cells and Cyst Walls." In The Cystic Kidney, 21–41. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0457-6_2.

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Chi, Lijun, and Norman Rosenblum. "Investigating Primary Cilia in Cultured Metanephric Mesenchymal Cells." In Kidney Development, 157–63. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-851-1_14.

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Guitynavard, Fateme, Seyed Mohammad Kazem Aghamir, and Diana Taheri. "Transplant and Kidney Repair." In Stem Cells in Urology, 101–17. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41476-4_8.

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Kuure, Satu. "Analysis of Migration in Primary Ureteric Bud Epithelial Cells." In Kidney Development, 147–55. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-851-1_13.

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Thowfeequ, Shifaan, and Odyssé Michos. "Isolation of High Quality RNA from Embryonic Kidney and Cells." In Kidney Development, 203–10. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-851-1_18.

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Liehr, Joachim G., and David A. Sirbasku. "Estrogen-Dependent Kidney Tumors." In Tissue Culture of Epithelial Cells, 205–34. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-4814-6_11.

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Morigi, Marina, Cinzia Rota, and Giuseppe Remuzzi. "Mesenchymal Stem Cells in Kidney Repair." In Mesenchymal Stem Cells, 89–107. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3584-0_5.

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Sorokin, Lydia, Gerd Klein, Gabriele Mugrauer, Lothar Fecker, Marja Ekblom, and Peter Ekblom. "Development of kidney epithelial cells." In Epithelial Organization and Development, 163–90. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-011-2354-9_6.

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Guggino, Sandra. "Channels in Kidney Epithelial Cells." In Ionic Channels in Cells and Model Systems, 207–20. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5077-4_13.

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Sharpe, Claire C. "Red Cells and the Kidney." In Primer on Nephrology, 827–42. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-76419-7_48.

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Conference papers on the topic "Kidney cells"

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de Koning, Constance. "Modified donor blood cells seem a promising option in kidney transplant recipients." In ASN Kidney Week 2022, edited by Rachel Giles. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/47c409cb.

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Afshar, Kourosh, B. Shadgan, and Baharak Tolouei. "Optical monitoring in kidney transplant." In Optical Interactions with Tissue and Cells XXXIII and Advanced Photonics in Urology, edited by Hyun Wook Kang, Ronald Sroka, Bennett L. Ibey, and Norbert Linz. SPIE, 2022. http://dx.doi.org/10.1117/12.2604261.

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"Are Normal Kidney Cells Influenced by Aspirin in Cell Culture?" In 5th International Conference on Biological, Chemical and Environmental Sciences. International Institute of Chemical, Biological & Environmental Engineering, 2016. http://dx.doi.org/10.15242/iicbe.c0316021.

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Boström, Anna-Karin, Martin Johansson, and Håkan Axelson. "Abstract 3368: Characterization of stem cell like cells in kidney cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3368.

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Kaewpaiboon, Sunisa, Titpawan Nakpheng, and Teerapol Srichana. "Biocompatibility of Polymyxin B Sulfate Based on Sodium Deoxycholate Sulfate Formulations with Kidney Cell Lines, Macrophage Cells, and Red Blood Cells." In 5th International Conference and Exhibition on Pharmaceutical Sciences and Technology 2022. Switzerland: Trans Tech Publications Ltd, 2022. http://dx.doi.org/10.4028/p-7490x3.

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Antibiotic-resistant has emerged without new drug challenges. Polymyxin B (PMB) was the last resort therapy for multiple-drug resistant Gram-negative bacteria. However, the toxicity of PMB including nephrotoxicity (61%) and neurotoxicity (7%) was dose-limitation. PMB-based sodium deoxycholate sulfate (SDCS) formulations were prepared in the 2-different mole ratios of SDCS to PMB (5:1 and 10:1). Particle size, zeta-potential, and drug content were evaluated. The biocompatibility of PMB formulations was investigated with normal human primary renal proximal tubule epithelial cells (PCS-400-010), human kidney epithelial cell lines (HEK 293T/17), human kidney cell lines (WT 9-12), macrophage-like cells (RAW 264.7) and red blood cells (RBC). PMB formulations had smaller particle sizes and lower zeta-potential when compared to PMB. PMB content presented from 97-100% after lyophilization. PMB-SDCS formulations revealed lower toxicity to cell lines than PMB, especially SDCS: PMB (5:1) and low lysis of RBC. PMB-SDCS mixture had better biocompatibility than those PMB and SDCS alone.

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Verhulst, Anja, Carl F. Verkoelen, Veerle P. Persy, and Marc E. De Broe. "CRYSTAL RETENTION CAPACITY OF HUMAN TUBULAR KIDNEY CELLS." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.330.

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Mackenzie, M. D., D. Choudhury, L. Paterson, R. R. Duncan, and A. K. Kar. "Femtosecond pumping of eGFP transfected human embryonic kidney cells." In 2013 Conference on Lasers and Electro-Optics Pacific Rim (CLEO-PR). IEEE, 2013. http://dx.doi.org/10.1109/cleopr.2013.6600621.

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Vitol, Elina A., Timothy P. Kurzweg, and Bahram Nabet. "Light scattering properties of kidney epithelial cells and nuclei." In Biomedical Optics 2006, edited by Robert R. Alfano and Alvin Katz. SPIE, 2006. http://dx.doi.org/10.1117/12.644863.

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"Is Normal Kidney Cells Viability Influenced by Estradiol Valerate Administration in Cell Culture?" In 2016 International Conference on Biological and Environmental Science. Universal Researchers, 2016. http://dx.doi.org/10.17758/ur.u0616227.

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Mehrvar, Shima, Mette Funding la Cour, Mahsa Ranji, Amadou K. S. Camara, and Meetha Medhora. "Optical cryoimaging for assessment of radiation-induced injury to rat kidney metabolic state." In Imaging, Manipulation, and Analysis of Biomolecules, Cells, and Tissues XVI, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2018. http://dx.doi.org/10.1117/12.2291555.

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Reports on the topic "Kidney cells"

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Sosa Munguía, Paulina del Carmen, Verónica Ajelet Vargaz Guadarrama, Marcial Sánchez Tecuatl, Mario Garcia Carrasco, Francesco Moccia, and Roberto Berra-Romani. Diabetes mellitus alters intracellular calcium homeostasis in vascular endothelial cells: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0104.

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Review question / Objective: What are the effects of diabetes mellitus on the calcium homeostasis in vascular endothelial cells? -To describe the effects of diabetes on the mechanisms that regulate intracellular calcium; -To describe other molecules/mechanisms that alters intracellular Ca2+ homeostasis. Condition being studied: Diabetes mellitus is a pathology with a high incidence in the population, characterized by an increase in blood glucose. People with diabetes are 2-4 times more likely to suffer from a cardiovascular complication, such as total or partial loss of sight, myocardial infarction, kidney failure, among others. Cardiovascular complications have been reported to derive from dysfunction of endothelial cells, which have important functions in blood vessels. In order to understand the etiology of this poor function of endothelial cells, it is necessary to study the molecular mechanisms involved in these functions, to identify the effects of diabetes and thus, develop new research that will mitigate the effects of this pathology.

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Semaan, Dima, and Linda Scobie. Feasibility study for in vitro analysis of infectious foodborne HEV. Food Standards Agency, September 2022. http://dx.doi.org/10.46756/sci.fsa.wfa626.

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Hepatitis E virus (HEV) is a member of the Hepeviridae family capable of infecting humans producing a range of symptoms from mild disease to kidney failure. Epidemiological evidence suggests that hepatitis E genotype III and IV cases may be associated with the consumption of undercooked pork meat, offal and processed products such as sausages [1]. A study carried out by the Animal Health and Veterinary Laboratories Agency (AHVLA), found hepatitis E virus contamination in the UK pork production chain and that 10% of a small sample of retail pork sausages were contaminated with the virus [2]. Furthermore, studies have confirmed the presence of HEV in the food chain and the foodborne transmission of Hepatitis E virus to humans [reviewed in 5]. Likewise, Scottish shellfish at retail [6] have also been found positive for HEV viral nucleic acid and some preliminary studies indicate that the virus is also detectable in soft fruits (L Scobie; unpublished data). There are current misunderstandings in what this data represents, and these studies have raised further questions concerning the infectivity of the virus, the processing of these foods by industry and the cooking and/or preparation by caterers and consumers. There are significant gaps in the knowledge around viral infectivity, in particular the nature of the preparation of food matrices to isolate the virus, and also with respect to a consistent and suitable assay for confirming infectivity [1,3]. Currently, there is no suitable test for infectivity, and, in addition, we have no knowledge if specific food items would be detrimental to cells when assessing the presence of infectious virus in vitro. The FSA finalised a comprehensive critical review on the approaches to assess the infectivity of the HEV virus which is published [3] recommending that a cell culture based method should be developed for use with food. In order to proceed with the development of an infectivity culture method, there is a requirement to assess if food matrices are detrimental to cell culture cell survival. Other issues that may have affected the ability to develop a consistent method are the length of time the virally contaminated sample is exposed to the cells and the concentration of the virus present. In most cases, the sample is only exposed to the cells for around 1 hour and it has been shown that if the concentration is less that 1x103 copies then infection is not established [3,5,10,11].

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Dominguez, Jesus, K. J. Kelly, and Jizhong Zhang. Intravenous Renal Cell Transplantation for Polycystic Kidney Disease. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada597871.

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Stewart, B. J. Mass Spectrometry Data Set for Renal Cell Carcinoma and Polycystic Kidney Disease Cell Models. Office of Scientific and Technical Information (OSTI), January 2017. http://dx.doi.org/10.2172/1342001.

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Eldar, Avigdor, and Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7575286.bard.

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In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.

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Banks, H. T., Karen M. Bliss, and Hien Tran. Modeling Red Blood Cell and Iron Dynamics in Patients with Chronic Kidney Disease. Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada556965.

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Pantuck, Allan. Early Diagnosis of Clear Cell Kidney Cancer via VHL/HIF Pathway-regulated Circulating microRNA. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada599473.

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Chou, Roger, Jesse Wagner, Azrah Y. Ahmed, Ian Blazina, Erika Brodt, David I. Buckley, Tamara P. Cheney, et al. Treatments for Acute Pain: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), December 2020. http://dx.doi.org/10.23970/ahrqepccer240.

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Objectives. To evaluate the effectiveness and comparative effectiveness of opioid, nonopioid pharmacologic, and nonpharmacologic therapy in patients with specific types of acute pain, including effects on pain, function, quality of life, adverse events, and long-term use of opioids. Data sources. Electronic databases (Ovid® MEDLINE®, PsycINFO®, Embase®, the Cochrane Central Register of Controlled Trials, and the Cochrane Database of Systematic Reviews) to August 2020, reference lists, and a Federal Register notice. Review methods. Using predefined criteria and dual review, we selected randomized controlled trials (RCTs) of outpatient therapies for eight acute pain conditions: low back pain, neck pain, other musculoskeletal pain, neuropathic pain, postoperative pain following discharge, dental pain (surgical or nonsurgical), pain due to kidney stones, and pain due to sickle cell disease. Meta-analyses were conducted on pharmacologic therapy for dental pain and kidney stone pain, and likelihood of repeat or rescue medication use and adverse events. The magnitude of effects was classified as small, moderate, or large using previously defined criteria, and strength of evidence was assessed. Results. One hundred eighty-three RCTs on the comparative effectiveness of therapies for acute pain were included. Opioid therapy was probably less effective than nonsteroidal anti-inflammatory drugs (NSAIDs) for surgical dental pain and kidney stones, and might be similarly effective as NSAIDs for low back pain. Opioids and NSAIDs were more effective than acetaminophen for surgical dental pain, but opioids were less effective than acetaminophen for kidney stone pain. For postoperative pain, opioids were associated with increased likelihood of repeat or rescue analgesic use, but effects on pain intensity were inconsistent. Being prescribed an opioid for acute low back pain or postoperative pain was associated with increased likelihood of use of opioids at long-term followup versus not being prescribed, based on observational studies. Heat therapy was probably effective for acute low back pain, spinal manipulation might be effective for acute back pain with radiculopathy, acupressure might be effective for acute musculoskeletal pain, an opioid might be effective for acute neuropathic pain, massage might be effective for some types of postoperative pain, and a cervical collar or exercise might be effective for acute neck pain with radiculopathy. Most studies had methodological limitations. Effect sizes were primarily small to moderate for pain, the most commonly evaluated outcome. Opioids were associated with increased risk of short-term adverse events versus NSAIDs or acetaminophen, including any adverse event, nausea, dizziness, and somnolence. Serious adverse events were uncommon for all interventions, but studies were not designed to assess risk of overdose, opioid use disorder, or long-term harms. Evidence on how benefits or harms varied in subgroups was lacking. Conclusions. Opioid therapy was associated with decreased or similar effectiveness as an NSAID for some acute pain conditions, but with increased risk of short-term adverse events. Evidence on nonpharmacological therapies was limited, but heat therapy, spinal manipulation, massage, acupuncture, acupressure, a cervical collar, and exercise were effective for specific acute pain conditions. Research is needed to determine the comparative effectiveness of therapies for sickle cell pain, acute neuropathic pain, neck pain, and management of postoperative pain following discharge; effects of therapies for acute pain on non-pain outcomes; effects of therapies on long-term outcomes, including long-term opioid use; and how benefits and harms of therapies vary in subgroups.

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Funkenstein, Bruria, and Cunming Duan. GH-IGF Axis in Sparus aurata: Possible Applications to Genetic Selection. United States Department of Agriculture, November 2000. http://dx.doi.org/10.32747/2000.7580665.bard.

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Many factors affect growth rate in fish: environmental, nutritional, genetics and endogenous (physiological) factors. Endogenous control of growth is very complex and many hormone systems are involved. Nevertheless, it is well accepted that growth hormone (GH) plays a major role in stimulating somatic growth. Although it is now clear that most, if not all, components of the GH-IGF axis exist in fish, we are still far from understanding how fish grow. In our project we used as the experimental system a marine fish, the gilthead sea bream (Sparus aurata), which inhabits lagoons along the Mediterranean and Atlantic coasts of Europe, and represents one of the most important fish species used in the mariculture industry in the Mediterranean region, including Israel. Production of Sparus is rapidly growing, however, in order for this production to stay competitive, the farming of this fish species has to intensify and become more efficient. One drawback, still, in Sparus extensive culture is that it grows relatively slow. In addition, it is now clear that growth and reproduction are physiological interrelated processes that affect each other. In particular sexual maturation (puberty) is known to be closely related to growth rate in fish as it is in mammals, indicating interactions between the somatotropic and gonadotropic axes. The goal of our project was to try to identify the rate-limiting components(s) in Sparus aurata GH-IGF system which might explain its slow growth by studying the ontogeny of growth-related genes: GH, GH receptor, IGF-I, IGF-II, IGF receptor, IGF-binding proteins (IGFBPs) and Pit-1 during early stages of development of Sparus aurata larvae from slow and fast growing lines. Our project was a continuation of a previous BARD project and could be divided into five major parts: i) obtaining additional tools to those obtained in the previous project that are necessary to carry out the developmental study; ii) the developmental expression of growth-related genes and their cellular localization; iii) tissue-specific expression and effect of GH on expression of growth-related genes; iv) possible relationship between GH gene structure, growth rate and genetic selection; v) the possible role of the IGF system in gonadal development. The major findings of our research can be summarized as follows: 1) The cDNAs (complete or partial) coding for Sparus IGFBP-2, GH receptor and Pit-1 were cloned. Sequence comparison reveals that the primary structure of IGFBP-2 protein is 43-49% identical to that of zebrafish and other vertebrates. Intensive efforts resulted in cloning a fragment of 138 nucleotides, coding for 46 amino acids in the proximal end of the intracellular domain of GH receptor. This is the first fish GH receptor cDNA that had been cloned to date. The cloned fragment will enable us to complete the GH - receptor cloning. 2) IGF-I, IGF-II, IGFBP-2, and IGF receptor transcripts were detected by RT-PCR method throughout development in unfertilized eggs, embryos, and larvae suggesting that these mRNAs are products of both the maternal and the embryonic genomes. Preliminary RT-PCR analysis suggest that GH receptor transcript is present in post-hatching larvae already on day 1. 3) IGF-1R transcripts were detected in all tissues tested by RT-PCR with highest levels in gill cartilage, skin, kidney, heart, pyloric caeca, and brain. Northern blot analysis detected IGF receptor only in gonads, brain and gill cartilage but not in muscle; GH increased slightly brain and gill cartilage IGF-1R mRNA levels. 4) IGFBP-2 transcript were detected only in liver and gonads, when analyzed by Northern blots; RT-PCR analysis revealed expression in all tissues studied, with the highest levels found in liver, skin, gonad and pyloric caeca. 5) Expression of IGF-I, IGF-II, IGF-1R and IGFBP-2 was analyzed during gonadal development. High levels of IGF-I and IGFBP-2 expression were found in bisexual young gonads, which decreased during gonadal development. Regardless of maturational stage, IGF-II levels were higher than those of IGF-L 6) The GH gene was cloned and its structure was characterized. It contains minisatellites of tandem repeats in the first and third introns that result in high level of genetic polymorphism. 7) Analysis of the presence of IGF-I and two types of IGF receptor by immunohistochemistry revealed tissue- and stage-specific expression during larval development. Immunohistochemistry also showed that IGF-I and its receptors are present in both testicular and ovarian cells. Although at this stage we are not able to pinpoint which is the rate-limiting step causing the slow growth of Sparus aurata, our project (together with the previous BARD) yielded a great number of experimental tools both DNA probes and antibodies that will enable further studies on the factors regulating growth in Sparus aurata. Our expression studies and cellular localization shed new light on the tissue and developmental expression of growth-related genes in fish.

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Hochman, Ayala, Thomas Nash III, and Pamela Padgett. Physiological and Biochemical Characterization of the Effects of Oxidant Air Pollutants, Ozone and Gas-phase Nitric Acid, on Plants and Lichens for their Use as Early Warning Biomonitors of these Air Pollutants. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7697115.bard.

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Introduction. Ozone and related oxidants are regarded as the most important phytotoxic air pollutant in many parts of the western world. A previously unrecognized component of smog, nitric acid, may have even greater deleterious effects on plants either by itself or by augmenting ozone injury. The effects of ozone on plants are well characterized with respect to structural and physiological changes, but very little is known about the biochemical changes in plants and lichens exposed to ozone and/or HNO3. Objectives.To compare and contrast the responses of crop plants and lichens to dry deposition of HNO3 and O3., separately, and combined in order to assess our working hypothesis that lichens respond to air pollution faster than plants. Lichens are most suitable for use as biomonitors because they offer a live-organism-based system that does not require maintenance and can be attached to any site, without the need for man-made technical support systems. Original Immediate aims To expose the tobacco (Nicotiana tabacum L.) cultivar Bel-W3 that is ozone supersensitive and the ozone sensitive red kidney bean (Phaseolusvulgaris) and the lichen Ramalinamenziesii to controlled HNO3 and O3 fumigations and combined and to follow the resulting structural, physiological and biochemical changes, with special reference to reactive oxygen species related parameters. Revised. Due to technical problems and time limitations we studied the lichen Ramalinamenziesii and two cultivar of tobacco: Bel-W3 that is ozone supersensitive and a resistant cultivar, which were exposed to HNO3 and O3 alone (not combined). Methodology. Plants and lichens were exposed in fumigation experiments to HNO3 and O3, in constantly stirred tank reactors and the resulting structural, physiological and biochemical changes were analyzed. Results. Lichens. Exposure of Ramalinamenziesiito HNO3 resulted in cell membrane damage that was evident by 14 days and continues to worsen by 28 days. Chlorophyll, photosynthesis and respiration all declined significantly in HNO3 treatments, with the toxic effects increasing with dosage. In contrast, O3 fumigations of R. menziesii showed no significant negative effects with no differences in the above response variables between high, moderate and low levels of fumigations. There was a gradual decrease in catalase activity with increased levels of HNO3. The activity of glutathione reductase dropped to 20% in thalli exposed to low HNO3 but increased with its increase. Glucose 6-phosphate dehydrogenase activity increase by 20% with low levels of the pollutants but decreased with its increase. Tobacco. After 3 weeks of exposure of the sensitive tobacco cultivar to ozone there were visible symptoms of toxicity, but no danmage was evident in the tolerant cultivar. Neither cultivar showed any visible symptoms after exposure to HNO3.In tobacco fumigated with O3, there was a significant decrease in maximum photosynthetic CO2 assimilation and stomatal conductance at high levels of the pollutant, while changes in mesophyll conductance were not significant. However, under HNO3 fumigation there was a significant increase in mesophyll conductance at low and high HNO3 levels while changes in maximum photosynthetic CO2 assimilation and stomatal conductance were not significant. We could not detect any activity of the antioxidant enzymes in the fumigated tobacco leaves. This is in spite of the fact that we were able to assay the enzymes in tobacco leaves grown in Israel. Conclusions. This project generated novel data, and potentially applicable to agriculture, on the differential response of lichens and tobacco to HNO3 and O3 pollutants. However, due to experimental problems and time limitation discussed in the body of the report, our data do not justify yet application for a full, 4-year grant. We hope that in the future we shall conduct more experiments related to our objectives, which will serve as a basis for a larger scale project to explore the possibility of using lichens and/or plants for biomonitoring of ozone and nitric acid air pollution.

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