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Academic literature on the topic 'WNT5A'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 January 2025

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Journal articles on the topic "WNT5A"

1

Anido, Urbano, Vanessa Medina Villaamil, Guadalupe Aparicio Gallego, et al. "Analysis of the expression of Wnt signaling ligands in metastatic renal cell carcinomas tissue samples." Journal of Clinical Oncology 30, no. 15_suppl (2012): e15077-e15077. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e15077.

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e15077 Background: Renal cell carcinomas (RCC) constitute a morphologically and genetically heterogeneous tumor.Wnt proteins are a large family of secreted glycoproteins that activate intracellular signal transduction pathways to control a wide variety of cellular processes such as determination of cell fate, proliferation, migration, and polarity.Wnt signalling may be playing a central role during RCC development. Methods: To characterize Wnt signalling activity in RCC, we gathered 48 tumor samples from patients diagnosed with metastatic RCC between years 2006 and 2011. Expression levels of Wnt family members (Wnt1, Wnt2, Wnt3a, Wnt4, Wnt5a, Wnt7a, and Wnt9a) were examined by real-time PCR and immunohistochemistry in tumor and normal tissue from removed kidneys. Results: Wnt1 and Wnt5a were up-regulated in clear cell RCC being their relative expression 2.4.103 (Wnt1) and 4.102 (Wnt5a) times higher in renal tumor tissue than in normal tissue. One-way ANOVA test showed Wnt3a and Wnt4 as the best protein markers to distinguish clear cell RCC (F=3.95, p=0.010 and F=3.05, p=0.029, respectively). Wnt1 and Wnt7a were over-expressed in those cases which had undergone nefrectomy (Mann-Whitney U test p=0.065 and p=0.056 respectively). Finally, Wnt2 protein level was associated with those patients with high risk prognosis (Kruskal-Wallis test p=0.001). Conclusions: Our results indicate that Wnt3a and Wnt4 are potentially useful immunohistochemical markers for the differential diagnosis between clear cell RCC and other subtypes of RCC and also suggest a role for Wnt2 as a high risk prognosis marker.

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Nemeth, Michael, and David Bodine. "Wnt5a Inhibits Wnt3a-Mediated HSC Differentiation." Blood 106, no. 11 (2005): 2271. http://dx.doi.org/10.1182/blood.v106.11.2271.2271.

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Abstract Activation of the canonical Wnt signaling pathway by Wnt3a has been implicated in hematopoietic stem cell (HSC) self-renewal (Reya et al., Nature, 2003). Wnt5a has been observed to inhibit Wnt3a signaling (Topol et al., J Cell Biol, 2004). We hypothesized that Wnt3a and 5a act as antagonists on HSC function. 1 x 106 lineage negative cells (lin−) were cultured for 4 days in the presence of 50 ng/ml SCF and Flt3L (control) plus 100 ng/ml rmWnt3a and/or 500 ng/ml rmWnt5a (all factors added on day 0 and day 2). Control lin− cell numbers expanded more than lin− cells cultured with Wnt3a, 5a, or both (control 8.3 ± 0.3-fold; Wnt3a 6.9 ± 0.2-fold (p &lt; .01); Wnt5a 4.8 ± 0.2-fold (p &lt; .001); Wnt3a and 5a 2.6 ± 0.6-fold (p &lt; .001); n = 3). After 4 days, cells were analyzed for myeloid colony formation. Control cells and cells cultured in Wnt3a had similar numbers of CFU-GM/5000 lin− cells (control 13.1 ± 11.1; Wnt3a 21.8 ± 15.3; p = .21; n = 8), while cells cultured in Wnt5a and Wnt3a and 5a had 2-fold and 5.9-fold more CFU-GM/5000 lin− cells than control (Wnt 5a 26.8 ± 13.3 (p = .04); Wnt3a and 5a 77.9 ± 48.3 (p &lt; .01); n = 8). To analyze repopulating ability, 4 x 105 lin− Ly5.1 cells, cultured under the same conditions, were transplanted with 2 x 106 Ly5.2 bone marrow cells into lethally-irradiated Ly5.2 recipients. 16 weeks after transplant, repopulation by control lin− cells increased 2-fold compared to lin− cells cultured in Wnt3a or Wnt5a (control 7.3 ± 3.8%; Wnt3a 3.37 ± 1.2% (p &lt; .01); Wnt5a 3.6 ± 1.1% (p &lt; .01); n = 9-10). However, lin− cells cultured in Wnt3a and 5a showed normal repopulating activity (n = 10; 8.7 ± 5.3%; p = .52). 1 x 104 HSCs (lin−, c-kitHI, Sca-1HI, IL-7Rα −) were cultured for 6 days with SCF, Flt3L, Wnt3a and 5a (factors added on day 0 and day 3) as described above. Control HSC numbers expanded more than HSCs cultured with Wnt3a, Wnt 5a, or both (control 20.7 ± 10.4-fold; Wnt 3a 7.0 ± 4.1-fold (p = .05); Wnt5a 1.7 ± 1.7-fold (p = .01); Wnt3a and 5a 1.2 ± 1.0-fold (p &lt; .01); n = 4). Similar numbers of control HSCs and HSCs cultured with Wnt3a or 5a were lin+ (control 21.7 ± 0.2%; Wnt 3a 15.4 ± 5.3% (p = .10); Wnt5a 14.4 ± 5.2% (p = .07); n = 3). However, culturing HSCs with Wnt3a and 5a resulted in a 50% decrease in the number of lin+ cells compared to control (12.3 ± 2.0% (p = .001)). Cultured Ly5.1 HSCs were transplanted with Ly5.2 bone marrow cells at a 1:100 ratio. There was no difference in repopulation between control HSCs and HSCs cultured with Wnt3a (control 5.8 ± 6.1%; Wnt3a 3.6 ± 0.4%; p = .43; n = 5). To examine the effects of enforced expression of Wnt ligands in HSCs, 5-FU treated bone marrow was transduced with Wnt3a-IRES-GFP, Wnt5a-IRES-dsRED, or IRES-GFP retroviral vectors. Sorted IRES-GFP+, Wnt3a-GFP+ and Wnt5a-dsRed+ cells (Ly5.1) were transplanted with equal numbers of mock-transduced cells and 3 x 105 Sca-1− bone marrow cells (Ly5.2) into lethally-irradiated Ly5.2 mice. 16 weeks later, recipients of IRES-GFP+ and Wnt5a-dsRed+ cells contained a similar number of engrafted cells expressing the vector (3.4 ± 1.8% GFP+ Ly5.1 and 3.5 ± 0.4% dsRed+ Ly5.1 respectively; n = 8). In contrast, no GFP+ Ly5.1 cells were detected in Wnt3a-GFP+ recipients (n = 8). 33.4 ± 3.7% of bone marrow cells were Ly5.1+ indicating successful engraftment and retroviral DNA was detected by PCR, suggesting that transduction had occurred but that only cells in which the vector was silenced survived. We conclude that activation of the canonical Wnt pathway in HSCs promotes differentiation of primitive hematopoietic cells and that other signals, such as Wnt5a, are required to maintain the balance between HSC differentiation and self-renewal.

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3

Abe, Akihiro, Yosuke Niwa, Jinglan Xu, et al. "Analysis of the Role of Wnt Signaling for the Interaction between Leukemia Cells and Stroma." Blood 110, no. 11 (2007): 4314. http://dx.doi.org/10.1182/blood.v110.11.4314.4314.

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Abstract Wnt signaling plays an important role in hematopoietic stem cell self-renewal and proliferation. Recent results also revealed that an aberrant activation of Wnt signaling has been related with hematological malignancies. We have previously reported a stroma-dependent human leukemia cell line, TRL-01, which could not be maintained by any cytokines without stroma or on fibronectin-coated plate although they periodically stimulated the proliferation. We here analyzed the role of Wnt signaling on the cell-adhesion, proliferation and survival of this cell line. TRL-01 was maintained on human bone marrow stroma cell line, hTERT. The apoptosis of TRL-01 on hTERT was suppressed by Wnt-receptor competitor, secreted Frizzled related protein (sFRP)-1, or Rho kinase inhibitor, Y29632 but not by specific inhibitor of canonical pathway, DKK-1. However, the apoptosis of TRL-01 without hTERT was not affected by sFRP-1, Y29632 or DKK-1. These results suggest that survival of TRL-01 on stroma was regulated by non-canonical pathway of Wnt signaling. Next, the effects of Wnt3A, 5A and 10B on TRL-01 were analyzed by establishing hTERT transduced with Wnt3A, 5A or 10B genes. Wnt3A is known as an important factor for the stimulation of self-renewal and proliferation of hematopoietic stem cells, and Wnt5A and 10B were reported to be expressed in B-ALL. When TRL-01 was cocultured with hTERT/Wnt3A or 10B, adhesion was reduced and β-catenin was significantly increased. The condition medium from hTERT/Wnt3A or 10B also stimulates the accumulation of β-catenin but inhibited the survival and proliferation of TRL-01. Wnt5A did not have any significant effects. These results suggest that Wnt3A and 10B stimulate canonical pathway with accumulation of β-catenin but negatively regulate the survival and proliferation of TRL-01. Comparing the expression pattern of Wnt transcripts of TRL-01 and hTERT by RT-PCR, Wnt5A, 5B and 14 were found to be dominantly expressed in hTERT. The role of Wnt5B and 14 for the interaction between TRL-01 and hTERT remains to be elucidated.

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Bolzoni, Marina, Paola Storti, Daniela Guasco, et al. "The Activation of Wnt5a-Mediated Non Canonical Wnt Signaling in Human Bone Marrow Osteoprogenitor Cells Increases Osteoblastogenesis and Counterbalances the Inhibitory Effect of Myeloma Cells on Ror2/FZD5 Expression,." Blood 118, no. 21 (2011): 3928. http://dx.doi.org/10.1182/blood.v118.21.3928.3928.

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Abstract Abstract 3928 Multiple Myeloma (MM) is characterized by the impairment of osteogenic differentiation of bone marrow (BM) mesenchymal stromal cells (BMSC) and osteoblast suppression. Canonical Wnt signal pathway is critical in the regulation of bone formation. However recent evidences suggest that non-canonical Wnt activation by Wnt5a, rather than canonical one by Wnt3a stimulates the osteogenic properties of BMSC. Non-canonical Wnt signaling, mainly activated by Wnt5a, is transduced through FZD receptor (FDZ5) and Ror2 co-receptor to several cascades such as Disheveled pathways involving the Rho family small GTPases or the Ca++ dependent pathways/PKC involving the nuclear factor of activated T cells (NFATc). Actually, the effect of MM cells on non-canonical Wnt signaling and the role of the activation of this pathway on MM-induced osteoblastic exhaustion are still unknown and have been investigated in this study. First we checked the expression of non-canonical Wnt related molecules by BMSC and osteoprogenitor cells (PreOB) and found that both cells expressed Wnt5a but lack of express Wnt1, Wnt3a and Wnt8. The presence of the Wnt5a receptors FZD2 and FZD5 was also detected in both cell types as well as of Ror2. Interestingly we found that osteogenic differentiation of BMSC towards preOB significantly increased Ror2 and FZD5 expression. Secondly, we performed a series of co-culture between PreOB and MM cells using either IL-6 dependent (XG-1), and independent (JJN3) human myeloma cell lines or purified primary CD138+ MM cells. We found that XG-1 and CD138+ MM cells inhibit Ror2 and FZD5 expression in PreOB and consistently the activity of NFATc1 at nuclear level. Thereafter the activation of non-canonical WNT pathway in PreOB, checked by the intracytoplasmatic increase of Ca++influx, phospho-PKC expression and NFATc1 activity, was induced either by Wnt5a treatment or by Wnt5a overexpression through a lentivirus vector. Ror2 overexpression was also performed by lentivirus vector in PreOB. The transcriptional profiles of both PreOB overexpressing Wnt5a and Ror2 have been evaluated by GeneChip® HG-U133Plus 2.0 arrays. The raw intensity signals were extracted from CEL files and normalized using the RMA package for Bioconductor and custom GeneAnnot-based Chip Definition Files in R software. We found that Wnt5a treatment as well as Wnt5a overexpression significantly increased osteogenic differentiation and the expression of the osteogenic markers alkaline phosphatase and collagen I in PreOB. Consistently with these observations, we also demonstrated that siRNA-mediated Wnt5a silencing inhibited these osteogenic markers in the same cell type. Moreover we found that the activation of non-canonical WNT signal pathway in PreOB, blunted the inhibitory effect of MM cells on the osteogenic differentiation process in co-culture. Finally, we show that Ror2 overespression in PreOB activated non-canonical Wnt signaling, increased osteogenic differentiation and restored the osteogenic properties of PreOB in co-culture with MM cells. In conclusion, our data indicate that activation of non-canonical Wnt5a/Ror2 pathway in BM osteoprogenitor cells increases osteogenic differentiation and counterbalances the inhibitory effect of MM cells suggesting that modulation of Wnt5/Ror2 pathway in the microenvironment could be a target for MM bone disease. Disclosures: Bolzoni: Celgene Italy: Research Funding. Giuliani:Celgene: Research Funding; Novartis: Research Funding.

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Ahmad, Samar, and Liliana Attisano. "Wnt5a Promotes Axon Elongation in Coordination with the Wnt–Planar Cell Polarity Pathway." Cells 13, no. 15 (2024): 1268. http://dx.doi.org/10.3390/cells13151268.

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The establishment of neuronal polarity, involving axon specification and outgrowth, is critical to achieve the proper morphology of neurons, which is important for neuronal connectivity and cognitive functions. Extracellular factors, such as Wnts, modulate diverse aspects of neuronal morphology. In particular, non-canonical Wnt5a exhibits differential effects on neurite outgrowth depending upon the context. Thus, the role of Wnt5a in axon outgrowth and neuronal polarization is not completely understood. In this study, we demonstrate that Wnt5a, but not Wnt3a, promotes axon outgrowth in dissociated mouse embryonic cortical neurons and does so in coordination with the core PCP components, Prickle and Vangl. Unexpectedly, exogenous Wnt5a-induced axon outgrowth was dependent on endogenous, neuronal Wnts, as the chemical inhibition of Porcupine using the IWP2- and siRNA-mediated knockdown of either Porcupine or Wntless inhibited Wnt5a-induced elongation. Importantly, delayed treatment with IWP2 did not block Wnt5a-induced elongation, suggesting that endogenous Wnts and Wnt5a act during specific timeframes of neuronal polarization. Wnt5a in fibroblast-conditioned media can associate with small extracellular vesicles (sEVs), and we also show that these Wnt5a-containing sEVs are primarily responsible for inducing axon elongation.

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Mastelaro de Rezende, Marina, Giselle Zenker Justo, Edgar Julian Paredes-Gamero, and Reinoud Gosens. "Wnt-5A/B Signaling in Hematopoiesis throughout Life." Cells 9, no. 8 (2020): 1801. http://dx.doi.org/10.3390/cells9081801.

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Wnt signaling is well-known to play major roles in the hematopoietic system, from embryogenesis to aging and disease. In addition to the main β-catenin-dependent pathway, it is now clear that Wnt5a and the structurally related Wnt5b are essential for hematopoiesis, bone marrow colonization and the final steps of hematopoietic stem cell (HSC) maturation via β-catenin-independent signaling. Wnt5a and Wnt5b ligands prevent hematopoietic exhaustion (by maintaining quiescent, long-term HSCs), induce the proliferation of progenitors, and guide myeloid development, in addition to being involved in the development of aging-related alterations. The aim of this review is to summarize the current knowledge on these roles of Wnt5a and Wn5b signaling in the hematopoietic field.

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Minami, Yosuke, Yosuke Niwa, Akihiro Abe, Fumihiko Hayakawa, and Tomoki Naoe. "Wnt Signaling Is Associated with Anti-Apoptosis in the Interaction Between Acute Myeloid Leukemia Cells and Stromal Cells." Blood 120, no. 21 (2012): 1366. http://dx.doi.org/10.1182/blood.v120.21.1366.1366.

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Abstract Abstract 1366 Recent studies have revealed that strength of the Wnt signaling pathway regulates normal hematopoiesis including hematopoietic stem cells, and aberrant activation of the pathway is involved in the development of several types of leukemias. In the bone marrow microenvironment, stromal cells are rich sources of cytokines and some secreted cytokines have been observed to block induction of cell death in myeloid leukemia cells exposed to chemotherapy. Here, we examined the role of the Wnt signaling pathway on cell-adhesion, proliferation and survival of the stroma-dependent human AML cell line, TRL-01 cells, which we previously established (Ninomiya, et al. Cancer Gen Cyto, 2006). TRL-01 cells were maintained in the co-culturing with the hTERT-transduced human bone marrow stroma cell line, HTS cells, and cell death of TRL-01 cells was induced after removal of HTS cells. Treatment with the Wnt-receptor competitor, secreted Frizzled related protein (sFRP)-1, or the Rho kinase inhibitor, Y29632 (previously reported as an inhibitor of the non-canonical Wnt downstream pathway), but not with the specific inhibitor of the canonical Wnt pathway (DKK-1) induced apoptosis in dose-dependent manners in TRL-01 cells co-cultured with HTS cells. These results suggested that the non-canonical pathway of Wnt signaling might regulate survival of TRL-01 on the stromal cells. Next, we comprehensively investigated transcripts of the Wnt pathway components (10 Frizzleds, 2 LRPs, and 18 Wnts) in TRL-01 cells and HTS cells using RT-PCR. Transcripts of Wnt5A and Wnt9A were expressed in TRL-01 cells, but not in HTS cells. Moreover, the cell death of TRL-01 cells after removal of HTS cells was partially prevented by additional treatment with Wnt5A or Wnt9A not by other Wnt molecules such as Wnt5B. On the other hand, treatment with Wnt3A induced activated nuclear beta-catenin using Western-blotting, however, did not contribute to the survival of TRL-01 cells without the stromal co-culturing. Moreover, we are investigating regulation of the anti-apoptotic downstream pathway molecules in TRL-01 cells as well as effects of other inhibitors targeted for the Wnt signaling. We are also examining expressions of Wnt pathway components in primary AML bone marrow cells and other human bone marrow stroma cell lines such as HS-5 cells. These results imply association of Wnt5A and Wnt9A with anti-apoptosis in the interaction between AML cells and stromal cells, and a possible therapeutic target of AML for overcoming the resistance to chemotherapy in the bone marrow microenvironment. Disclosures: Naoe: Chugai Pharma: Research Funding; Novartis Pharma: Research Funding; Kyowa-Hakko Kirin: Research Funding.

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Nishita, Michiru, Sa Kan Yoo, Akira Nomachi, et al. "Filopodia formation mediated by receptor tyrosine kinase Ror2 is required for Wnt5a-induced cell migration." Journal of Cell Biology 175, no. 4 (2006): 555–62. http://dx.doi.org/10.1083/jcb.200607127.

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The receptor tyrosine kinase Ror2 plays important roles in developmental morphogenesis. It has recently been shown that Ror2 mediates Wnt5a-induced noncanonical Wnt signaling by activating the Wnt–JNK pathway and inhibiting the β-catenin–TCF pathway. However, the function of Ror2 in noncanonical Wnt signaling leading to cell migration is largely unknown. We show, using genetically different or manipulated cultured cells, that Ror2 is critical for Wnt5a-induced, but not Wnt3a-induced, cell migration. Ror2-mediated cell migration requires the extracellular cysteine-rich domain (CRD), which is the binding site for Wnt5a, and the cytoplasmic proline-rich domain (PRD) of Ror2. Furthermore, Ror2 can mediate filopodia formation via actin reorganization, irrespective of Wnt5a, and this Ror2-mediated filopodia formation requires the actin-binding protein filamin A, which associates with the PRD of Ror2. Intriguingly, disruption of filopodia formation by suppressing the expression of either Ror2 or filamin A inhibits Wnt5a-induced cell migration, indicating that Ror2-mediated filopodia formation is essential for Wnt5a-induced cell migration.

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Mumford, Petey W., Matthew A. Romero, Xuansong Mao, et al. "Cross talk between androgen and Wnt signaling potentially contributes to age-related skeletal muscle atrophy in rats." Journal of Applied Physiology 125, no. 2 (2018): 486–94. http://dx.doi.org/10.1152/japplphysiol.00768.2017.

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We sought to determine whether age-related gastrocnemius muscle mass loss was associated with parallel decrements in androgen receptor (AR) or select Wnt signaling markers. To test this hypothesis, serum-free and total testosterone (TEST) and gastrocnemius AR and Wnt signaling markers were analyzed in male Fischer 344 rats that were 3, 6, 12, 18, and 24 mo (mo) old ( n = 9 per group). Free and total TEST was greatest in 6 mo rats, and AR protein and Wnt5 protein levels linearly declined with aging. There were associations between Wnt5 protein levels and relative gastrocnemius mass ( r = 0.395, P = 0.007) as well as AR and Wnt5 protein levels (r = 0.670, P < 0.001). We next tested the hypothesis that Wnt5 affects muscle fiber size by treating C2C12-derived myotubes with lower (75 ng/ml) and higher (150 ng/ml) concentrations of recombinant Wnt5a protein. Both treatments increased myotube size ( P < 0.05) suggesting this ligand may affect muscle fiber size in vivo. We next tested if Wnt5a protein levels were androgen-modulated by examining 10-mo-old male Fischer 344 rats ( n = 10–11 per group) that were orchiectomized and treated with testosterone-enanthate (TEST-E); trenbolone enanthate (TREN), a nonaromatizable synthetic testosterone analogue; or a vehicle (ORX only) for 4 wk. Interestingly, TEST-E and TREN treatments increased Wnt5a protein in the androgen-sensitive levator ani/bulbocavernosus muscle compared with ORX only ( P < 0.05). To summarize, aromatizable and nonaromatizable androgens increase Wnt5a protein expression in skeletal muscle, age-related decrements in muscle AR may contribute Wnt5a protein decrements, and our in vitro data imply this mechanism may contribute to age-related muscle loss. NEW & NOTEWORTHY Results from this study demonstrate androgen and Wnt5 protein expression decrease with aging, and this may be a mechanism involved with age-related muscle loss.

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Pacheco, Ivan I., and R. John MacLeod. "CaSR stimulates secretion of Wnt5a from colonic myofibroblasts to stimulate CDX2 and sucrase-isomaltase using Ror2 on intestinal epithelia." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 4 (2008): G748—G759. http://dx.doi.org/10.1152/ajpgi.00560.2007.

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To understand whether extracellular calcium-sensing receptor (CaSR) expression on colonic myofibroblast cells (18Co) contributed to epithelial homeostasis, we activated the CaSR with 5 mM Ca2+, screened by RT-PCR Wnt family members, and measured their secretion. Transcripts for Wnt 1, 2, 2b, 3a, 4, and 7a were either absent or unchanged whereas Wnt3 decreased and Wnt5a increased. We assessed Wnt5a secretion by Western blot. High Ca2+ (5 mM) substantially increased Wnt5a secretion; small interfering RNA (siRNA) against the CaSR reduced this to constitutive amounts. Expression of Wnt5a plasmid but not Wnt1 or Wnt3a increased caudal homeodomain factor CDX2 transcripts and protein in HT-29 adenocarcinoma cells. Wnt5a increased activity of a sucrase-isomaltase (SI) promoter in Caco-2BBE cells. Wnt5a protein stimulation of CDX2 transcripts and protein and SI reporter were increased by overexpression of wild-type Ror2, a Wnt5a receptor, and reduced with siRNA against Ror2. CaSR activation of HT-29 cells increased Ror2 protein expression. Ror2 protein was expressed in mouse jejunum from crypt base to villus tip and in the colon on surface epithelia. Our results show that activation of a G protein-coupled receptor, the CaSR, stimulates secretion of Wnt5a from myofibroblasts. Stimulation of epithelia by the CaSR increased the expression of a receptor for Wnt5a, the tyrosine kinase Ror2, suggesting existence of a unique paracrine relationship for CDX2 homoeostasis in the intestine and revealing new contributions of CaSR-activated myofibroblasts to intestinal stem cell niche microenvironments.

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Dissertations / Theses on the topic "WNT5A"

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Thomson, Craig. "WNT5A in Malignant Peripheral Nerve Sheath Tumors." University of Cincinnati / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1613742042185276.

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Allen, John C. "FGF4 Induced Wnt5a Gradient in the Limb Bud Mediates Mesenchymal Cell Directed Migration and Division." BYU ScholarsArchive, 2013. https://scholarsarchive.byu.edu/etd/4309.

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The AER has a vital role in directing embryonic limb development. Several models have been developed that attempt to explain how the AER directs limb development, but none of them are fully supported by existing data. I provide evidence that FGFs secreted from the AER induce a gradient of Wnt5a. I also demonstrate that limb mesenchyme grows toward increasing concentrations of Wnt5a. We hypothesize that the changing shape of the AER is critical for patterning the limb along the proximal to distal axis. To better understand the pathway through which Wnt5a elicits its effects, we have performed various genetic studies. We demonstrate that Wnt5a does not signal via the Wnt/β-catenin pathway. However, we show that Wnt5a mutants share many common defects with Vangl2 mutants suggesting that Wnt5a signals through the Wnt/planar cell polarity (PCP) pathway.

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Christman, Mark Andrew II. "WNT5A EXPRESSION IN HUMAN AND MURINE ATHEROSCLEROTIC LESIONS." Ohio University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1180659149.

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Bhatt, Pooja. "Understanding and Exploiting Wnt5a and GSK3 Signaling in Inflammatory Disease." Ohio University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1365012252.

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Bauer, Matthieu. "Biological functions and signaling cascades of novel isoforms of WNT5A." Paris 11, 2010. http://www.theses.fr/2010PA11T001.

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Jenty, Marion. "Rôle de la signalisation LRP1/Wnt5a dans le métabolisme du cholestérol." Thesis, Strasbourg, 2016. http://www.theses.fr/2016STRAJ025/document.

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L’athérosclérose débute par l’accumulation de cholestérol dans les cellules des parois artérielles, formant des plaques d’athéromes. LRP1 protège contre la maladie en inhibant l’accumulation intracellulaire de cholestérol et nous avions montré qu’une signalisation Wnt5a était impliquée dans cette inhibition. Le projet de thèse consistait à caractériser les mécanismes moléculaires de cette inhibition et à vérifier l’effet athéroprotecteur de Wnt5a. Nous avons montré in vitro et in vivo que Wnt5a inhibe l’accumulation de cholestérol via la stimulation de son export et l’inhibition de sa synthèse endogène. Nous avons ensuite observé que l’invalidation de Wnt5a spécifiquement dans les CMLv de souris LDLR-/- conduit à une augmentation des lésions athéromateuses après un régime riche en cholestérol, confirmant alors son rôle athéroprotecteur. Nos travaux ont ainsi permis de révéler le potentiel de Wnt5a en tant que cible thérapeutique dans le traitement contre l’athérosclérose<br>Protects against intracellular cholesterol accumulation and we identified the secreted protein Wnt5a as a partner of this inhibitory effect of LRP1. The aim of this thesis is to determine the molecular mechanisms by which the LRP1/Wnt5a signaling pathway prevents cholesterol accumulation in cells and to study the antiatherogenic potential of Wnt5a. We first showed in vitro and in vivo that Wnt5a decreases cellular cholesterol content by stimulating its efflux through the induction of cholesterol transporters expression and by down-regulating the expression of HMGCoA-reductase. Then we used mice deleted for Wnt5a specifically in smooth muscle cells, which present more atherosclerotic lesions than control mice after a high cholesterol diet. This confirms that Wnt5a protects against atherosclerosis and could be an interesting therapeutic target in the treatment of the disease

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Kummitha, China Malakondaiah. "Applied Molecular Recognition of HECA-452 and Wnt5a in Pathological Inflammation." Ohio University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1267990823.

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Susman, Michael Wen. "The Wnt5a-Ror Signaling Pathway in the Morphogenesis of the Embryo." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:23845401.

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Embryonic development is orchestrated by relatively few conserved core developmental signaling pathways that are used reiteratively to grow, specify and shape all tissues in the body into their final functional forms. The Wnt5a signaling pathway is necessary to shape and extend various tissues during morphogenesis, but how Wnt5a signals within cells has long remained unclear and controversial. Through loss-of-function experiments in mice, we demonstrate that the Ror family of receptors mediates Wnt5a-dependent processes in vivo at multiple stages of embryonic development. Of previously proposed mediators of Wnt5a-Ror signaling, we identify Dishevelled phosphorylation, but not the inhibition of β-catenin-dependent transcription or the activation of the JNK pathway, as a physiological target of Wnt5a-Ror signaling. To further understand the molecular mechanisms underlying Wnt5a-Ror function, we performed a proteomic mass spectrometry screen to identify additional mediators of the Wnt5a-Ror pathway. This screen led to the discovery that Kif26b, an atypical and largely uncharacterized member of the kinesin superfamily, is part of an evolutionarily conserved signaling cassette with Wnt5a and Ror proteins during embryonic development. Interestingly, we found that Kif26b protein exhibits a polarized subcellular localization at the trailing edge of cultured mesenchymal cells and functions to promote the migration of these cells. Wnt5a triggers the degradation of Kif26b by a proteasome-dependent mechanism and negatively regulates cell migration in a Kif26b- dependent manner. Together, these findings identify a new noncanonical Wnt5a-Ror-Kif26b signaling pathway that links extracellular signaling to cytoskeletal changes that influences the movement, polarity and shape of developing tissues, and pathological situations where this signaling may be dysregulated.<br>Medical Sciences

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Pietilä, I. (Ilkka). "The role of Dkk1 and Wnt5a in mammalian kidney development and disease." Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526207216.

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Abstract This thesis focuses on mammalian kidney development and in particular on the question of how two Wnt signalling pathway genes, an antagonistic Dkk1 and an agonistic ligand Wnt5a, regulate the process. Wnts are secreted ligands that are involved in many developmental processes, including gonadal differentiation and kidney development, but also in various diseases and malformations. Wnts form a large signalling family containing 19 different glycoprotein ligands in mammals. Wnt signalling occurs via two different intracellular pathways. A canonical pathway proceeds via beta-catenin, and a non-canonical pathway utilizes other signalling molecules. Dkk1 is an antagonist of the canonical pathway and Wnt5a is considered a ligand that activates the non-canonical signalling pathway. As part of the thesis, I have studied the role of Dkk1 in kidney morphogenesis using a conditional mouse model, in which the gene is deleted in a cell specific manner from the collecting ducts. Dkk1 deficiency increased renal papilla growth and the risk of hydronephrosis. Research pointed out that the lack of Dkk1 in the collecting ducts increased cell proliferation and disturbed the balance of canonical Wnt signalling, which led to an overgrowth of renal papilla. This led to functional phenotypes including increased water reabsorption and changes in ion secretion/absorption. These changes are most likely due to altered Wnt7b signalling. The second part of the thesis examines the role of the non-canonical Wnt5a gene in kidney development with a conventional knock out mouse model. At the time work began on the thesis, no corresponding kidney phenotype had been published. The primary finding in kidneys lacking Wnt5a was an altered basement membrane organization of the collecting ducts and glomeruli. The phenotype is most likely the reason behind morphological phenotypes which vary from bilateral kidney agenesis to duplex collecting system. Notably, during the course of this study we found a mutation in the human WNT5A gene of a CAKUT patient. This is the first time Wnts have been shown to organize kidney development via basement membrane formation<br>Tiivistelmä Tämän väitöskirjan tarkoituksena on ollut tutkia munuaisen kehitystä ja kuinka kaksi Wnt-signalointireitin geeniä, signalointia estävä Dkk1 ja signalointia edistävä Wnt5a säätelevät sitä. Wnt ligandit ovat eritettäviä signaalimolekyylejä, jotka ovat osallisina monissa kehitysbiologissa prosesseissa kuten sukupuolen määräytymisessä ja munuaisen kehityksessä. Myös monissa taudeissa on havaittu muuntuneita Wnt geenien tuottotasoja. Wnt-geenit muodostava suuren signalointimolekyyliperheen, johon lukeutuu 19 jäsentä nisäkkäillä ja Wnt-signointi on jaettu perinteisesti kahteen signalointiryhmään. Dkk1 on kanonisen Wnt-signaloinnin estäjä ja Wnt5a:ta pidetään pääsaantiöisesti ei-kanonisena Wnt-ligandina. Väitöskirjassani olen tutkinut Dkk1 geenin toimintaa kohdennetussa Dkk1-poistogeenisessä hiiressä, jossa geenin toiminta on poistettu spesifisesti munuaisen kokoojaputkista. Dkk1:n puutos johtaa munuaisen papillan kasvuun ja lisää riskiä hydronefroksen muodostumiseen. Tutkimukset osoittivat että Dkk1:n puutos aiheuttaa lisääntynyttä solujakautumista kokoojaputkissa, jolloin Wnt-signaloinnin muutos aiheuttaa papillan ylikasvua. Ylikasvusta seuraa lisääntynyttä veden takaisin imeytymistä ja muutoksia ionien erittämisessä ja takaisin imeytymisessä. Todennäköisimmin muutokset johtuvat muuntuneesta Wnt7b signaloinnista, jota Dkk1 normaalisti säätelee. Väitöskirjan toisessa osassa tutkittiin ei-kanonisen reitin Wnt5a ligandin roolia munuaisen kehityksessä käyttäen poistogeenistä hiirimallia, jossa Wnt5a:n roolia munuaisenkehityksessä ei ollut julkaistu työn aloituksen aikaan. Wnt5a:n puutoksen havaittiin vaikuttavan tyvikalvon järjestymiseen kokoojaputkissa ja munuaiskeräsessä. Tyvikalvon häiriö on todennäköisin syy morfologisiin muutoksiin, jotka vaihtelevat molempien munuaisen puuttumisesta kaksois-kokoojatiehyen muodostumiseen. Työssä osoitetaan ensimmäistä kertaa kuinka Wnt-signalointireitin proteiinit säätelevät munuaisen kehitystä tyvikalvon muodostuksen kautta

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Low, Keri Lynn. "FGF4 and Wnt5a/PCP signaling promote limb outgrowth by polarizing limb mesenchyme /." Diss., CLICK HERE for online access, 2006. http://contentdm.lib.byu.edu/ETD/image/etd1612.pdf.

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Books on the topic "WNT5A"

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Blumenthal, Antje. Expression von Wnt5a in humanen Makrophagen: Induktion und Funktion bei der Abwehr mykobakterieller Infektionen. 2003.

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Book chapters on the topic "WNT5A"

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O'Connell, Michael P., Amanda D. French, Poloko D. Leotlela, and Ashani T. Weeraratna. "Assaying Wnt5A-Mediated Invasion in Melanoma Cells." In Methods in Molecular Biology. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-249-6_19.

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Matsumoto, Shinji, and Akira Kikuchi. "Regulation of Focal Adhesion Dynamics by Wnt5a Signaling." In Methods in Molecular Biology. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-61779-510-7_17.

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Hall, Christine M., Amaka C. Offiah, Francesca Forzano, Mario Lituania, Gen Nishimura, and Valérie Cormier-Daire. "Robinow Syndrome, Recessive and Dominant Types, ROR2-, NXN-, WNT5A-, DVL1-, DVL3- and FZD2-Related." In Fetal and Perinatal Skeletal Dysplasias, 2nd ed. CRC Press, 2024. http://dx.doi.org/10.1201/9781003166948-55.

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Rajamannan, Nalini M. "Wnt3a-Lrp5 mediated Bicuspid Aortic Valve Disease." In Molecular Biology of Valvular Heart Disease. Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6350-3_9.

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Hall, Christine M., Amaka C. Offiah, Francesca Forzano, Mario Lituania, Gen Nishimura, and Valérie Cormier-Daire. "Limb Reduction Syndrome (Al-Awadi Raas-Rothschild Limb-Pelvis Hypoplasia-Aplasia), WNT7A-Related." In Fetal and Perinatal Skeletal Dysplasias, 2nd ed. CRC Press, 2024. http://dx.doi.org/10.1201/9781003166948-120.

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Heasley, Lynn E., and Robert A. Winn. "Analysis of Wnt7a-Stimulated JNK Activity and cJun Phosphorylation in Non-Small Cell Lung Cancer Cells." In Methods in Molecular Biology. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-249-6_14.

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Bryce, Daniel, and Seungchan Kim. "Planning Interventions for Gene Regulatory Networks as Partially Observable Markov Decision Processes." In Handbook of Research on Computational Methodologies in Gene Regulatory Networks. IGI Global, 2010. http://dx.doi.org/10.4018/978-1-60566-685-3.ch023.

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In this chapter, a computational formalism for modeling and reasoning about the control of biological processes is explored. It comprises five main sections: a survey of related work, a background on methods (including discussion of the Wnt5a gene regulatory network, the coefficient of determination method for deriving gene regulatory network models, and the partially observable Markov decision process model and its role in modeling intervention planning problems), a main section on the approach taken (including algorithms for solving the intervention planning problems and techniques for representing components of the problems), an empirical evaluation of the intervention planning algorithms on synthetic and the Wnt5a gene regulatory networks, and a conclusion and future directions section. The techniques described present a promising avenue of future research in reasoning algorithms for improved scalability in planning interventions in gene regulatory networks.

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Chakraborty, Arijit, Shreyasi Maity, and Malini Sen. "Wnt5A Signaling Antagonizes Leishmania donovani Infection." In Vector-Borne Diseases - Recent Developments in Epidemiology and Control. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.87928.

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Konopelski Snavely, Sara E., Srisathya Srinivasan, Courtney A. Dreyer, Jia Tan, Kermit L. Carraway, and Hsin-Yi Henry Ho. "Non-canonical WNT5A-ROR signaling: New perspectives on an ancient developmental pathway." In Current Topics in Developmental Biology. Elsevier, 2023. http://dx.doi.org/10.1016/bs.ctdb.2023.01.009.

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Endo, Mitsuharu, Michiru Nishita, Masanori Fujii, and Yasuhiro Minami. "Insight into the Role of Wnt5a-Induced Signaling in Normal and Cancer Cells." In International Review of Cell and Molecular Biology. Elsevier, 2015. http://dx.doi.org/10.1016/bs.ircmb.2014.10.003.

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Conference papers on the topic "WNT5A"

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Daud, Tariq, Aarti Parmar, Amanda Sutcliffe, et al. "The role of WNT5a in Th17 asthma." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3416.

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Singla, A., K. Peters, S. Reuter, et al. "Role of Wnt5a signals in allergic asthma." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1945.

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Bakker, Elvira R. M., Wendy van Veelen, Werner Helvensteijn, Ernst J. Kuipers, and Ron Smits. "Abstract 2408: Generation of an inducible Wnt5a transgenic mouse model to study the contribution of increased Wnt5a expression to intestinal tumor growth." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2408.

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Bakker, Elvira, Werner Helvensteijn, Wendy van Veelen, Ernst J. Kuipers, and Ron Smits. "Abstract 4156: Generation of an inducible Wnt5a transgenic mouse model to study the contribution of increased Wnt5a expression to intestinal tumor growth." 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.am10-4156.

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Li, C., N. Peinado, S. M. Smith, et al. "Wnt5a Promotes Alveolar Type 1 Cell Differentiation During Lung Development." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5480.

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Li, C., S. M. Smith, J. C. Zhou, et al. "WNT5A Isoforms Are Dynamically Regulated in Lung Development and Fibrosis." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a2479.

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Kisel, W., S. Conrad, G. Furesi, et al. "High stromal WNT5A is an indicator for low risk prostate cancer." In Osteologie 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402854.

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Nisa, Silmy Aulia Rufiatin, Elhah Nailul Khasna, Dwi Listyorini, and Nursasi Handayani. "Ciprofloxacin down-regulates Wnt5a gene expression in chick embryo leg bud." In INVENTING PROSPEROUS FUTURE THROUGH BIOLOGICAL RESEARCH AND TROPICAL BIODIVERSITY MANAGEMENT: Proceedings of the 5th International Conference on Biological Science. Author(s), 2018. http://dx.doi.org/10.1063/1.5050151.

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Remtisch, L., G. Wiltberger, K. Schierle, et al. "Die Bedeutung des WNT5a/ROR2 Signalweges beim duktalen Adenokarzinom des Pankreas." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1604963.

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Bitler, Benjamin G., Jasmine P. Nicodemus, Hua Li, et al. "Abstract 1230: Wnt5a-dependent induction of senescence suppresses epithelial ovarian cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1230.

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Reports on the topic "WNT5A"

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Wright, Alec, Susan Miranda, and Gustavo Miranda-Carboni. The Co-expression of ROR1 and FZD2 in WNT5B Signaling in Osteosarcoma. University of Tennessee Health Science Center, 2024. http://dx.doi.org/10.21007/com.lsp.2024.0022.

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