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Dissertations / Theses on the topic 'Mammary gland involution'
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Hughes, Katherine. "Inflammation and remodelling in mammary gland involution." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607688.
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Kreuzaler, Peter Anton. "Cell death modalities in mammary gland involution." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609378.
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Treisman, Loren Lee. "The role of the PARbZips in mammary gland involution." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614361.
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Charifou, Elsa. "Characterization and impact of cellular senescence during mammary gland involution." Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS559V2.pdf.
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La sénescence est une réponse à un stress biologique, caractérisée par un arrêt stable du cycle cellulaire. Néanmoins, les cellules restent métabolliquement actives et acquièrent un phenotype sécrétoire associé à la sénescence, avec la production d’un sécrétome complexe composé de cytokines, chémiokines, facteurs de croissance et modulateurs du remodelage de la matrice extracellulaire. La sénescence est associée à de nombreux processus pathologiques, comme la tumorigénèse et le vieillessement. Cependant, où, quand et comment la sénescence contribue aux processus physiologiques reste méconnu. Pour répondre à cette question, nous avons tiré profit de la glande mammaire (GM), un organe avec une plasticité remarquable pendant le développement post-natal. L’involution de la GM est l’un des évenements majeurs de mort cellulaire et de remodelage tissulaire chez les mammifères, lorsque les cellules épithéliales produisant le lait sont éliminées et que la GM retourne à son état pré-grossesse, attendant la prochaine gestation. Au cours de ma thèse, nous avons montré que la sénescence était induite transitoirement pendant la phase irréversible de l’involution. De plus, le programme de sénescence apparaissait spécifiquement dans les cellules luminales productrices de lait et corrélait à l’expression de l’inhibiteur du cycle cellulaire p16. En parallèle, nous avons établi un nouveau modèle d’organoides pour mimer la gestation, la lactation et l’involution de la GM. Dans ce modèle ex-vivo, nous avons aussi relever la présence de cellules sénescentes strictement lors du processus d’involution. Pour évaluer l’impact biologique de la sénescence in vivo, nous avons utilisé une méthode de scellement des mamelons pour découpler les phases réversible et irréversible de l’involution. Nous avons dévoilé une association étroite entre le sevrage des hormones lactogéniques qui a lieu lors de la seconde phase d’involution, et l’induction du programme de sénescence. Pour mieux définir les rôles physiologiques de la sénescence pendant l’involution, nous avons traités des souris avec de l’ABT-263, un composé sénolytique induisant l’apoptose des cellules sénescentes. Nous avons observé une altération du remodelage tissulaire suite à l’élimination des cellules sénescentes, avec des alvéoles résiduelles plus larges et un remplissage adipocytaire retardé. De plus, dans des organoides provenant de souris transgéniques p16-3MR, nous avons éliminé les cellules sénescentes avec succès grâce à l’administration de ganciclovir, ce qui a retardé le processus d’involution. Dans leur ensemble, les modèles in vivo et ex-vivo suggèrent un rôle important de la sénescence pour moduler la phase de remodelage tissulaire dans l’involution de la GM. Enfin, le processus d’involution est intiment lié avec le cancer du sein post-partum, un cancer diagnostiqué dans les 10 ans suivant une grossesse et associé à un mauvais pronostic. Explorer comment la sénescence impacte le microenvironnement lors de l’involution pourrait ainsi fournir de nouvelles connaissances pour mieux comprendre le cancer du sein post-partum<br>Cellular senescence is a biological stress response characterized by a stable cell cycle arrest. Nonetheless, cells remain metabolically active and acquire a senescence-associated secretory phenotype (SASP), a complex secretome composed of cytokines, chemokines, growth factors, and extracellular matrix remodeling modulators. Senescence is associated with various pathological processes, such as tumorigenesis and aging. However, it is unknown when, where and how senescence contributes to physiological processes. To answer this question, we took advantage of the mammary gland (MG), an organ with remarkable plasticity throughout postnatal development. The MG involution is one of the major mammalian cell death and tissue remodeling events, when milk-producing epithelial cells are removed, and the MG returns to its pre-gestation state, resting for further pregnancy. During my Ph.D., we showed that senescence was transiently induced during the irreversible phase of involution. The senescent program occurred specifically in the alveolar milk-producing luminal cells and correlated with the expression of the cell cycle inhibitor p16. In parallel, we established a novel organoid system to mimic MG gestation, lactation, and involution. In this ex-vivo model, we also highlighted the presence of senescent cells strictly during the involution-like process. To assess the biological impact of senescence in vivo, we used a teat sealing method to uncouple the reversible and irreversible phases of involution. We unveiled a close association between the withdrawal of lactogenic hormones occurring in the second phase of involution and the induction of the senescence program. To further define the physiological roles of senescence during involution, we treated mice with ABT-263, a senolytic compound inducing apoptosis of senescent cells. Interestingly, we observed an impaired tissue remodeling upon senescence elimination, with larger remaining alveolar structures and delayed adipocyte refilling. Moreover, in organoids from transgenic p16-3MR mice, we successfully removed senescent cells with ganciclovir and delayed the involution-like process. Taken together, both in vivo and ex-vivo models suggest an essential role of senescence in modulating the tissue remodeling phase of MG involution. Importantly, the involution process is intimately associated with postpartum breast cancer (PPBC), a cancer diagnosed within 10 years following delivery with a poor prognosis. Investigating how senescence impacts the microenvironment during the involution process might provide major insights to understand PPBC
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Staniszewska, Anna Dominika. "Roles of Stat3 in mammary gland development, involution and breast cancer." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610277.
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Anderson, Torri R. "Determination of expression of Fliz1 during involution of the mouse mammary gland." Thesis, Villanova University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=1565164.
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<p> Remodeling of the mouse mammary gland is a highly coordinated process that occurs after the removal of suckling pups from the mother. Involution, or shrinking of the mammary gland, after removal of the pups has been linked to apoptotic events within the mouse mammary tissue during forced weaning. Several transcription factors are hypothesized to be involved in this process. A transcription factor known as GATA-3, which was first identified in the thymus, is also important for maintenance of various tissue types within the mouse mammary gland; its loss leads to epithelial cell detachment and eventual death. Another transcription factor known as fetal zinc liver finger protein 1, or Fliz1, has been found to regulate GATA-3 in T-cells. This interaction had not been elucidated during involution in mouse mammary tissue. I hypothesized that Fliz1 is expressed at heightened levels during mouse mammary gland involution following forced weaning of pups, and that this expression correlates with a decrease in GATA-3 levels, with increased expression of the pro-apoptotic protein BAD. Using qRT-PCR, immunoblotting and immunohistochemistry I have shown that Fliz1 is indeed expressed in involuting mouse mammary gland tissue as well as several other tissue types. However, levels of Fliz1 remain fairly constant during involution. The findings also show that Cathepsin L, a known apoptotic marker for mammary gland involution, is substantially up-regulated during the process of mammary gland involution in the mouse. The study also revealed that GATA-3 levels as hypothesized decrease substantially during the process of mouse mammary gland involution, indicating that GATA-3 is required for maintenance of the mouse mammary gland.</p>
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Marshall, Aaron. "The Biology of Mammary Gland Serotonin Synthesis and Transport." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1251229830.
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Pai, Vaibhav Prakash. "Serotonin Regulation of Mammary Gland Involution and its Role in Breast Cancer Progression." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1237565289.
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Patel, Amita. "Transcriptional regulation of cathepsin L during mouse mammary gland involution a test of STAT3 involvement /." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432835.
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Stairiker, Patricia A. "The role of L in involution and the termination of lactation in the mouse mammary gland." Click here for download, 2007. http://proquest.umi.com/pqdweb?did=1075710531&sid=3&Fmt=2&clientId=3260&RQT=309&VName=PQD.
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Stairiker, Patricia A. "The role of cathepsin L in involution and the termination of lactation in the mouse mammary gland." Click here for download, 2006. http://wwwlib.umi.com/cr/villanova/fullcit?p1432836.
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Neoh, Kevin. "A study of the p50α/p55α phosphoinositide 3-kinase regulatory subunits in mammary gland involution". Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611285.
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Girnius, Nomeda A. "The cJUN NH2-terminal kinase pathway in mammary gland biology and carcinogenesis." eScholarship@UMMS, 2018. https://escholarship.umassmed.edu/gsbs_diss/961.
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The cJUN NH2-terminal kinase (JNK) pathway responds to environmental stresses and participates in many cellular processes, including cell death, survival, proliferation, migration, and genome maintenance. Importantly, genes that encode components of the JNK signaling pathway are frequently mutated in human breast cancer, but the functional consequence of these mutations in mammary carcinogenesis is unclear.
Anoikis – suspension-induced apoptosis – has been implicated in oncogenic transformation and tumor cell metastasis. Anoikis also contributes to lumen formation during mammary gland development and epithelial cell clearance during post-lactational involution. JNK is known to contribute to certain forms of cell death, but the role of JNK during anoikis was unclear. I examined the requirement of JNK in anoikis and discovered that JNK promotes cell death by transcriptional and post-translational regulation of pro-apoptotic BH3-only proteins. This conclusion suggested that JNK signaling may contribute to mammary gland remodeling during involution. Indeed, JNK deficiency in mammary epithelial cells disrupted the remodeling program of gene expression and delayed involution. Finally, I sought to understand the importance of JNK in mammary carcinogenesis. I found that JNK loss in the mammary epithelium was sufficient for genomic instability and tumor formation. Moreover, JNK loss in a model of breast cancer resulted in significantly accelerated tumor development. Collectively, these studies advance our understanding of the JNK pathway and breast biology, and provide insight that informs the design of therapeutic approaches that target the JNK signal transduction pathway.
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CATTANEO, LUCA. "Comprendere la messa in asciutta nella bovina da latte: approfondimenti su metabolismo e infiammazione." Doctoral thesis, Università Cattolica del Sacro Cuore, 2022. http://hdl.handle.net/10280/131852.
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La messa in asciutta sta diventando una fase sempre più importante del ciclo di lattazione. Rappresenta un evento stressante per la bovina da latte perché comporta diversi cambiamenti nella gestione e nella fisiologia degli animali. Eventi infiammatori in questa fase possono avere anche sulla lattazione successiva. Inoltre, l'elevata produzione di latte che viene raggiunta dalle vacche moderne in tarda gestazione può influenzare l'adattamento al periodo di asciutta e potrebbe compromettere la futura produttività e lo stato di salute degli animali. Inoltre, le forti richieste di ridurre l'uso di antibiotici nell’allevamento e la diffusione della terapia selettiva all’asciutta sollevano ulteriori preoccupazioni riguardo a questa fase.
Nella presente tesi è stato indagato l'effetto di condizioni infiammatorie sistemiche alla messa in asciutta sull'adattamento al successivo periparto. Quindi, è stato valutato un approccio di messa in asciutta selettiva, concentrandosi in particolare sulle risposte immunometaboliche e sulle implicazioni sulla successiva lattazione. Inoltre, è stata valutata con un approccio simile l'integrazione con un nutraceutico (Aloe arborescens Mill.). Successivamente, è stata analizzata l'espressione genica dei leucociti circolanti all’asciutta, per capire cosa accade a livello molecolare, confrontando vacche con diversa produzione di latte, e confermando gli effetti negativi dell'elevata produzione sulla risposta infiammatoria. Negli anni sono state proposte diverse strategie per ridurre gradualmente la produzione di latte prima dell'asciutta, favorendo l'avvio del processo di involuzione mammaria. Pertanto, sono stati valutati gli effetti della restrizione alimentare su produzione e metabolismo.<br>The dry-off is an important phase of the lactation cycle. It represents a stressful event for dairy cows because it includes several changes in animal management and physiology. Inflammatory events in this phase seem to have a carryover effect on the ensuing lactation. Moreover, the high milk yield still achieved by modern cows in late gestation can affect the adaptation to the non-lactating period and might impair future performance and health. Furthermore, the public demand to reduce antibiotic use in livestock and the spread of selective dry-cow therapy raise additional concerns about this phase.
In this thesis, the effect of systemic inflammatory conditions at dry-off on the adaptation to the subsequent calving has been investigated. Then, a selective dry-cow therapy approach was evaluated, particularly focusing on the immunometabolic responses and the implications on the ensuing early lactation. Moreover, to optimize this strategy, the supplementation of a nutraceutical (Aloe arborescens Mill.) has been tested with a similar approach. Furthermore, circulating leukocyte gene expression was analyzed at the turn of the dry-off, to understand what happens at a molecular level, comparing cows with different yields, and confirming the detrimental effect of high yield on the inflammatory response. Several strategies have been proposed over the years to gradually reduce milk yield before dry-off, promoting the beginning of the mammary involution process. Thus, we evaluated the effects of feed restriction on performance and metabolism.
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Bielke, Wolfgang. "Identification snd characterization of programmed cell death-associated genes during involution of the mammary and prostate glands /." [S.l.] : [s.n.], 1994. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Guenette, Robert S. "Gene expression during active cell death in involuting prostate and mammary gland: Cloning and characterization of regression-selected genes (RSG)." Thesis, University of Ottawa (Canada), 1995. http://hdl.handle.net/10393/9824.
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Following hormonal ablation in the rat ventral prostate (via castration) or rat mammary gland (after weaning) the epithelial cells of both glands are eliminated by active cell death during the regression of the glands. Several genes including TRPM-2, (testosterone repressed prostate message), RVP.1, fos, and myc, have been shown to be induced in the prostate during this process. We have investigated the expression of several other genes that may be associated with apoptosis, including tissue transglutaminase (tTGase), poly (ADP-ribose) polymerase (PARP), and heat shock protein 27 (Hsp27). Northern hybridization has been used to determine the steady-state mRNA levels of these genes in both the regressing prostate and mammary glands. The time course of induction has been compared to changes in the steady state levels of several control genes including prostate steroid binding protein (PSBP) (prostate), $\beta$-casein (mammary), $\alpha$-tubulin, and TRPM-2 (both prostate and mammary). A novel cross-screening approach first described by Wong et al., 1989 was used to clone and characterize genes other than those described above which were induced during the regression of both rat prostate and mammary gland. Two regression selected genes (RSG) refered to as RSG-2, and RSG-8, were isolated, and their role in the active cell death process has been investigated. RSG-2 is homologous to cathepsin B, a thiol protease that has been previously identified as one of the extracellular proteases that is activated in metastatic cells. RSG-8, is homologous to rat insulin like growth factor binding protein 5 (IGFBP-5), a member of a group of six related proteins that are known to mediate the effects of the growth factors IGF-I, and IGF-II. The steady state level of IGFBP-5 mRNA in the normal prostate is low but detectable. In the regressing prostate, the mRNA for IGFBP-5 mRNA is induced and its steady state peaks in the luminal epithelial cells of the prostate that undergo active cell death (ACD) between 3 and 4 days after castration. The gene is induced in a similar fashion in the regressing mammary gland following weaning. The expression of another IGFBP, namely IGFBP-2 contrasts that of IGFBP-5, with a high steady state level in both prostate and mammary gland, which increase only slightly during the regression process. The increase in mRNA steady-state levels for both IGFBP-2 and IGFBP-S were shown by in-situ hybridization to localize to the epithelial cells that are deleted during the regression process. The differential expression of IGFBP-2 and IGFBP-5 suggest that modulating the epithelial cells response to the IGF growth factors may influence the active cell death process in hormonally dependent tissues such as the prostate and mammary gland. (Abstract shortened by UMI.)
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Newton, Hamish Tazewell. "The dry period: the optimum time for cure: an investigation of the factors influencing the cure of intramammary infection in the involuting mammary gland." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492584.
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Mastitis is a major disease in the modern dairy cow with respect to both cow welfare and the quality and quantity of milk produced. The dry period is increasingly being recognised as a critical time point within the lactation cycle for the control of mastitis-causing pathogens.
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Yu, Ting-Chieh, and 余亭潔. "MMP-9 from PMN associate with cow mammary gland involution." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/73791771698889013311.
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碩士<br>中興大學<br>動物科學系所<br>95<br>An influx of polymorphonuclear neutrophils (PMN) immediately after drying-off was observed to increase the proportion of PMN of somatic cell counts (SCC) of bovine mammary gland. Matrix metalloproteinases (MMPs) involve in the remodeling of tissue under many physiological circumstances. PMN is the richest source of the MMP-9, which functions to degrade collagen Ⅳ of basement membrane proteins during tissue remodeling. It was also demonstrated that tumor necrosis factor-α (TNF-α) released by PMN can induce mitogen-activated protein kinase (MAPK) mediated-MMP-9 degranulation. The objectives of this study were to determine the involvement of MMP-9 in involution of cow mammary gland after drying-off and to assess the mechanisms by which MMP-9 might be regulated by TNF-α via autocrine/paracrine loop. Six cows were used to provide weekly mammary secretion samples from 0-3 weeks after milk-stasis. Skimmed mammary secretion were used to prepare serum and somatic cells to evaluate the alteration of content of MMP-9 and TNF-α in serum, the expression and activation of MAPK pathways of somatic cells after drying-off. Results show that SCC of mammary dry secretion abruptly increased at wk 1 and continued climbing up to wk 3. MMP-9 was not detected in regular milk but appeared at wk 0 and elevated significantly thereafter. MMP-2, on the other hand, was detected both in regular milk and dry secretion, only was higher during the latter period. The increasing MMP-9/MMP-2 ratio in mammary tissue after milk stasis suggests a greater contribution of MMP-9 to mammary involution. Content of 17kDa TNF-α in serum of dry secretion was lower than regular milk and decreased along the dry period. The expressions of MAPK family and TNF-α on somatic cells as revealed by Western blot show that less 17 kDa TNF-α relative to 26 kDa TNF-α was expressed on somatic cells of regular milk compared to that of dry glands, confirming that greater amount of 17 kDa TNF-α was released from somatic cells during lactation. The ratio of expression of phosphorylated to unphosphorylated MAPK family remained similar to wk 0 throughout dry period which suggest no MAPK pathway. Results of in vitro studies indicate that mammary dry secretion stimulated MMP-9 degranulation from PMN to 1.6 folds after 30 min incubation, which was partially abolished in the presence of p38 inhibitor but was not for anti-TNF-α antibody. A 6.1 folds of stimulatory effect on TNF-α release was observed under similar incubation environment, so did the effect of p38 inhibitor. It is postulated that the release of MMP-9 and TNF-α from PMN is partially mediated by MAPK pathway and is TNF-α autocrine/paracrine loop independent. In conclusion, SCC and MMP-9 in mammary lumen continuously increase after milk stasis of dairy cows implying their close association with mammary gland involution. The release of MMP-9 and TNF-α from somatic cells during mammary gland involution is partially mediated by activation of MAPK pathway to collaborate tissue remodeling and boost glandular immunity. The bioactive components of dry mammary secretion which promote these functions of somatic cells warrant further identification.
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DeCorby, Nicole. "Differential gene expression during early involution of the mouse mammary gland." 2005. http://hdl.handle.net/1993/20143.
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Hojilla, Carlo Vincent. "The role of TIMP3 in mammary gland morphogenesis, involution, inflammation, and tumourigenesis." 2006. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=449903&T=F.
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Weng, Ming-Huang, and 翁明煌. "Plasmin system and matrix metalloproteinases as indices of involution of goat mammary gland." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/91192850685262143060.
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碩士<br>國立中興大學<br>畜產學系<br>91<br>Plasminogen activator（PA）/plasmin system and matrix metalloproteins（MMPs）are vital proteases which breakdown extracellular matrix（ECM）and basement membrane. Large amount of proteolysis is required for tissue remodeling during involution of mammary gland. The present study explored the activity of PA/plasmin system at various lactation states. Furthermore their activities in plasma and milk neutrophils were also compared to establish the sources of variation in PA/plamsin activity in milk of goat.
Plasmin activity in milk of goat was significantly higher（P < 0.05）in involution stage（including gradual involution; GI and steady involution; SI）than lactation stage but not for plasma. Therefore, the change in plasmin activity of milk was not systemic. Plasmin seemed directly participate in ECM breakdown of mammary gland during involution, and served a very important role in tissue remodeling. Plasminogen activity in milk of SI stage was higher（P < 0.05） compare to those of very active latation（VL）, less active lactation and GI stage but not in plasma. Plasminogen might be supplied as abundant precursor of plasmin during involution of mammary gland. Urokinase-PA（uPA）activity in milk of goat displayed the similar tendency as plasmin and plasminogen. Since uPA activated plasminogen to plasmin that contributed the increased plasmin activity in mammary gland during involution.
Activities of MMP-2 and MMP-9 in milk of SI and GI were higher（P < 0.05）compare to those of VL and LL, but not in plasma. During involution, the increased activity of plasmin and uPA enhanced the activation of pro-MMP-9 and pro-MMP-2 in milk. Also, the release of MMP-9 from milk neutrophils was higher（P < 0.05） at involution stage compare to lactation stage. It is suggested that the increased activity of uPA during involution further stimulated the released of gelatinase from milk neutrophils. The results of zymography showed that plasmin in milk and plasma were approximately 75 kDa and 85 kDa in molecular weight, respectively. uPA in milk was approximately 60 kDa. The type of plasmin in milk of goats were slightly different from the 88 kDa plasmin of cow milk but the type of uPA in milk of these two species were similar.
Study of the expression of uPA and uPAR（uPA-receptor） in mammary tissue of dried goats using Western blot analysis indicated that both expressed mostly in plasma membrane. uPA bound to uPAR on cell membrane was enhanced in activity towards plasminogen activation and gelatinase release. Expressions of uPA and uPAR on neutrophils from milk were also increased during involution stage. uPA up-regulates its own expression via the uPAR pathway. Therefore, increase uPA in milk elevated, the expression of both uPA and uPAR on milk neutrophils.
The results of the present study suggest that the expression of uPA and uPAR in mammary tissue of involution satge increased to enhance the conversion of plasminogen to plasmin. Simultaneously, MMP-2 and MMP-9 activity in milk were also elevated by uPA. In turn, increase uPA activity in milk during involution stage stimulated uPA and uPAR expression on neutrophils which further released more MMP-9. Therefore, the cascades interplayed by PA/plasmin system and MMPs within mammary gland during involution work together to promote the process of tissue regression. Changes in activity of these proteases are reliable indicators of the extent of mammary involution.
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SHU, SUE HSIN, and 蘇鑫淑. "The immunoregulatory role of CD200 in the involuting mammary gland of ratsThe immunoregulatory role of CD200 in the involuting mammary gland of ratsThe immunoregulatory role of CD200 in the involuting mammary gland of rats." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/68398513379841614686.
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碩士<br>國防醫學院<br>生物及解剖學研究所<br>96<br>Abstract
Mammary gland involution is a highly complex multi-step process that is characterized by a high degree of epithelial cell death, redevelopment of the mammary adipose tissue and tissue remodeling. A significant infiltration of leukocytes and macrophages into the lumen and between the mammary epithelial cells is also a crucial process during involution that showed drastically altered expression of adhesion molecules. CD200 is an adhesion molecule belonging to immunoglobulin superfamily and well known as an immunosuppressive molecule. In our previous study, CD200 does exist on the myoepithelia of rat mammary glands and be closely related to the physical stages of the mammary epithelial cells. We hypothesize that myoepithelial CD200 may constitutively have an immunosuppressive influence on infiltrated leukocytes/macrophages during normal mammary involution to maintain an appropriate immune reaction. To verify this assumption, the evolution of immunomolecules during gland involution of rats will initially be examined. The neutralization with CD200 antiserum will then be applied to evidence the rigorous immune reaction and epithelial destruction after CD200 antibody ligation. Our preliminary data demonstrated that immune cells varied in distribution dependent on their immunomolecules and the stage of mammary regression. During the first 7 days mammary involution, CD45+ cells were mainly distributed at the intraepithelial site and increased in packing density with time through which their cell density per acinus and ROS were significantly declined. Antibody against CD200 to some extent reinforced the immune activity that showed an increased expression of ROS, immunomolecules and population of the immune cells and may lead to more advanced involution. The present data therefore suggested a constitutively immunosuppressive influence of myoepithelial cells on the immune cells during normal involution of rat mammary gland.
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su, Wen-jeng, and 蘇文正. "Apoptosis and peroxidation in the secretion of involuting goat mammary gland." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/10409556258994534521.
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碩士<br>國立中興大學<br>畜產學系<br>88<br>英文摘要
Apoptosis is a form of cell death which provides the organism with both the capability to remove specific cells during development and a way to continuously turnover cells in tissues. Oxidants such as oxygen free radicals may be essential biochemical intermediates in the progression of apoptosis. In the present study, involution of goat mammary gland following dry off was used as a model for researching apoptosis and antioxidants events. Mammary secretions were collected from goats in four different physiological stages：3 to 1 weeks before dry off（late）, 1 week following dry off（involution 1）, 2 weeks following dry off（involution 2）and 4 to 6 weeks after parturition（peak）. Cellular and non-cellular liquid parts of mammary secretion were separated（500×g, 10 min）and were used for assaying antioxidative enzymes superoxide dismutase（SOD）and glutathione peroxidase（GPx）and measurement of lipid peroxidation as represented by concentration of thiobarbituric acid reactive substances（TBARS）. Cell type and morphology as well as the manner and extent of DNA degradation were also observed.
Polymorphonuclear leukocyte（PMN）with an average diameter 10-15 μm was the major cell type in all stages. Mammary epithelial cell was identified immunohistochemically by fluorescence microscopy. Vacuoles and oligonucleosomal DNA laddering in ethidium bromide-stained gel indicated that cells loss by apoptosis occurred starting in late stage and most prominently during involution, but apparent not during peak stage. Direct microscopic somatic cell counts（DMSCC）for 1（56.8×105/ml）and 2（52.6×105/ml）weeks following dry off were significantly higher than those for late（28.2×105/ml）and peak（3.8×105/ml）stages. The contents of total cellular DNA（8.89mg/dl）and percentages of cellular DNA fragmentation（76﹪）during involution were higher than those of the rest stages. For non-cellular liquid of mammary secretion, SOD activity was the highest in stage involution 1（1.07 U/ml）, GPx was the highest during late stage（0.31 U/ml）. Concentrations of TBARS was the highest in stage involution 2. For the cellular part of mammary secretion, activities of SOD and GPx were significantly lower during involution than late and peak stages. No differences in concentrations of TBARS was observed for these four stages.
Concentrations of cellular TBARS was highly correlated with the percentages of DNA fragmentation（r＝0.33）and cellular DNA content（r＝0.40）. Cellular activities of SOD and GPx were negatively correlated with percentages of DNA fragmentation（r＝-0.38 ＆ -0.39）. Concentrations of TBARS and SOD activity in non-cellular mammary secretion was highly correlated with percentages of DNA fragmentation（r＝0.32 ＆ 0.47）.
In summary, during 1 to 2 weeks following dry off, there were significant elevation of DMSCC, total cellular DNA content, percentages of DNA fragmentation and concentrations of TBARS in mammary secretion. Meanwhile, activities of cellular SOD and GPx in mammary secretion were significantly depressed. Appearance of DNA laddering demonstrates the progression of apoptosis during involution. Finally, concentrations of TBARS in mammary secretion is a good index of mammary involution, and the lowering of antioxidative enzyme activities in cell of mammary secretion during involution probably caused DNA fragmentation therefore suggests a role of oxygen free radical in apoptosis of mammary involution.
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Chang, Yao-Wen, and 張耀文. "CD200 Distribution in Rat Mammary Glands during Resting, Pregnancy, Lactation and Involution." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/19453207447598594075.
Full textAbstract:
碩士<br>國防醫學院<br>生物及解剖學研究所<br>94<br>Abstract
In the present study, we demonstrated a similar CD200 expression in the myoepithelial cells of the mammary glands. Myoepithelial cells were well known to be altered morphologically under different hormonal conditions in a physiologic state correlative to the luminal epithelial cells. Indeed, our present study further showed a differential expression of myoepithelial CD200 in the rat mammary gland during resting, pregnancy, lactation and involution. CD200 is distributed at entire cytoplasmic membrane of myoepithelial cells in the virgin mammary gland. This expression is altered when rats are in pregnancy and myoepithelial CD200 is expressed only on the cytoplasmic membrane facing the basal lamina and absent on that facing the epithelium. The polarity of CD200 expression on myoepithelial cells is reversed during lactation. Interestingly, myoepithelial cells investing regressing alveoli of involuted glands showed a moderate but continuous CD200 immunoreactivity on the cytoplasmic membrane facing the basal lamina. Opposite degenerated epithelial cells, the immunoreactivity on the membrane is however intense but sporadic. Extended study on chronological changes of myoepithelial CD200 in the involuted glands showed an increased CD200 expression on myoepithelia that retracted their processes bearing more obvious protrusions with advance of the involution. At the final phase of mammary involution when the ducts and alveoli regressed towards a resting state, intense CD200 immunoreactivity was found at not only myoepithelia but some epithelial cells. The remarkable expression of epithelial CD200 was also evidenced in the mammary glands of 5-week-old pubertal rats that showed intense immunoreactivity on the cytoplasmic membrane including its apical modifications of major but not all epithelial cells. Interestingly, the outermost layer made up by cap cells of the terminal end buds has nerve possessed CD200. It is also true for epithelial cells of mammary glands during pregnancy, lactation and involution. These results indicated that myoepithelial cells of the mammary glands may be changed and related to the physiologic state of the epithelial cells by hormonal environments synchronizing the gland growth through in part CD200 adhesion molecules.