Nestin expression in repopulating mesangial cells promotes their proliferation

Daniel, Christoph; Albrecht, Heinz; Lüdke, Andrea; Hugo, Christian

doi:10.1038/labinvest.2008.5

Cited by 58 publications

(51 citation statements)

References 44 publications

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“…Consequently, experiments using 10 nM siRNA were shown. Downregulation of transgelin was evaluated by western-blot analysis as previously described 18 and cells were tested in proliferation and migration assays.…”

Section: Transfection With Transgelin Sirnamentioning

confidence: 99%

Transgelin is a marker of repopulating mesangial cells after injury and promotes their proliferation and migration

Daniel

Lüdke

Wagner

et al. 2012

Laboratory Investigation

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Mesangial cell (MC) migration is essential during glomerular repair and kidney development. The aim of the study was to identify marker/player for glomerular progenitor/reserve cells migrating into the glomerulus after MC injury and during glomerulogenesis in the rat. Experimental mesangial proliferative nephritis was induced in Sprague Dawley rats by intravenous injection of OX-7 antibody. We investigated mRNA expression profiles in isolated glomeruli from on days 0, 1, 2, 3, and 5 after induction of anti-Thy1 nephritis using Affymetrix microarray technology. Using self-organizing maps, transgelin was identified as a new marker for repopulating glomerular cells. Expression of transgelin during anti-Thy1 nephritis was investigated by northern blot, real-time PCR, western blot, and immunohistochemistry. Migration and proliferation assays using isolated MCs after transgelin knockdown by siRNA were performed to investigate the potential role of transgelin during glomerular repopulation. Transgelin mRNA was not detected in healthy glomeruli. It was strongly upregulated during the repopulation process starting on day 1, continued to be increased until day 5 and disappeared on day 7. Transgelin was specifically expressed at the edge of the migratory front during glomerular repopulation as indicated by transgelin/OX-7 double staining. Transgelin expression was similar in migrating vs non-migrating MCs in vitro. Blocking of transgelin expression by siRNA treatment resulted in inhibition of MC migration and proliferation. Transgelin was also expressed in MCs during glomerulogenesis and in biopsies from patients with IgA nephritis. In conclusion, transgelin in the kidney is upregulated in repopulating MCs in vivo and supports their migratory and proliferative repair response after injury.

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Section: Transfection With Transgelin Sirnamentioning

confidence: 99%

Transgelin is a marker of repopulating mesangial cells after injury and promotes their proliferation and migration

Daniel

Lüdke

Wagner

et al. 2012

Laboratory Investigation

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“…Despite the plethora of data supporting the premise that nestin expression identified a stem cell phenotype, recent studies have detected the intermediate filament protein in numerous non-stem cell populations during physiological growth and pathological remodeling. Nestin was highly expressed in developing skeletal myofibers and downregulated following maturation, upregulated in endothelial cells during reparative angiogenesis, and induced in mesangial cells following injury and in scar myofibroblasts and cardiac myocyte-like cells bordering the peri-infarct/infarct region of the ischemically damaged rodent and human heart (1,3,4,7,9,11,24,25,31,32). However, in contrast to neural progenitor/stem cells, expression of the intermediate filament protein in skeletal myofibers and endothelial cells was driven by the first intron of the nestin gene (1,42,43).…”

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confidence: 99%

“…However, in contrast to neural progenitor/stem cells, expression of the intermediate filament protein in skeletal myofibers and endothelial cells was driven by the first intron of the nestin gene (1,42,43). Biologically, nestin expression was reported to play a seminal role in cell proliferation (4,9,37,38).Vascular remodeling is a hallmark feature of hypertension, characterized in part by the proliferation and hypertrophy of vascular smooth muscle cells (13). A recent study reported that a subpopulation of vascular smooth muscle cells residing in the normal rat aorta expressed the intermediate filament protein nestin and was actively engaged in the cell cycle (27).…”

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confidence: 99%

Nestin upregulation characterizes vascular remodeling secondary to hypertension in the rat

Tardif

Hertig

Duquette

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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The present study tested the hypothesis that vessel remodeling secondary to hypertension was characterized by nestin upregulation in vascular smooth muscle cells. Two weeks after suprarenal abdominal aorta constriction of adult male Sprague-Dawley rats, elevated mean arterial pressure increased the media area and thickness of the carotid artery and aorta and concomitantly upregulated nestin protein levels. In the normal adult rat carotid artery, nestin immunoreactivity was observed in a subpopulation of vascular smooth muscle cells, and the density significantly increased following suprarenal abdominal aorta constriction. Filamentous nestin was detected in cultured rat carotid arteryand aorta-derived vascular smooth muscle cells and an analogous paradigm observed in human aorta-derived vascular smooth muscle cells. ANG II and EGF treatment of vascular smooth muscle cells stimulated DNA and protein synthesis and increased nestin protein levels. Lentiviral short-hairpin RNA-mediated nestin depletion of carotid artery-derived vascular smooth muscle cells inhibited peptide growth factor-stimulated DNA synthesis, whereas protein synthesis remained intact. These data have demonstrated that vessel remodeling secondary to hypertension was characterized in part by nestin upregulation in vascular smooth muscle cells. The selective role of nestin in peptide growth factor-stimulated DNA synthesis has revealed that the proliferative and hypertrophic responses of vascular smooth muscle cells were mediated by divergent signaling events. nestin; carotid artery; aorta; hypertension; vascular remodeling DURING THE DEVELOPMENT of the central nervous system (CNS), a population of neuroepithelial stem cells was initially identified via expression of the intermediate filament protein nestin (8,18). Nestin is a 240-kDa protein and a member of the class VI family of intermediate filament proteins, and, in contrast to other classes, it is unable to self-assemble and form homodimers because of a short NH 2 terminus (37, 39). Therefore, nestin will form heterodimers with other intermediate filament proteins, including vimentin and desmin (37). The promoter region upstream of exon 1 of the nestin gene does not contain any identifiable elements regulating expression. However, the nestin gene does contain regulatory elements in the various intron regions that drive expression in a cell-specific manner (37). In neural progenitor/stem cells, nestin expression is independently regulated by restricted enhancer elements identified in the second intron (43). In humans, a highly conserved region that directed expression was also identified in the second intron of the nestin gene (21). However, nestin expression driven by the second intron was not limited to CNSresident stem cells, since a transgenic mouse containing the 5.8-kb fragment of the promoter region and the 1.8-kb fragment of the second intron of the rat nestin gene linked to the reporter green fluorescent protein (GFP) identified progenitor/ stem cell populations in the skin, skeletal mus...

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“…Currently, the regular methodology is to use a combination of FGF-2 and EGF co-factors to culture NSCs in vitro (9)(10)(11)(12). In this study, we used the same method to culture NSCs and confirmed the cell identify using immunohistochemical staining for nestin, a protein that disappears along with the differentiation and maturation of the neural epithelium (13)(14)(15)(16). CaM has been proven to be a versatile Ca 2+ -binding protein and exists in neural cells in a large quantity (17)(18)(19).…”

Section: Discussionmentioning

confidence: 89%

Involvement of calmodulin and actin in directed differentiation of rat cortical neural stem cells into neurons

Shi¹

2011

Int J Mol Med

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Abstract. Calmodulin (CaM) is a multifunctional receptor of intercellular Ca 2+, which under different physiological conditions or at different developmental stages plays different roles in different tissues and cells. This study aimed to investigate the involvement of spatial expression and coexistence of CaM and actin in directed differentiation of rat cortical neural stem cells (NSCs) into neurons. Immunohistochemistry, RT-PCR and immunofluorescence dual-labeling technology was conducted to investigate the temporal and spatial pattern of CaM and actin proteins in neuron-oriented cortical NSC differentiation. Confocal laser scanning microscopy (CLSM) was used to observe changes of the coexistence in protein expression. Our results showed that cortical NSCs expressed and showed localized CaM and actin in a well-defined temporal order. In the process of rat neuron-oriented cerebral cortical NSC differentiation, CaM displayed a similar expression pattern with actin in the development of neurons, that is, both proteins extended into neurites following the sprouting and growth of neurons. These results suggest that the temporal and spatial pattern of CaM and actin expression is comparable to the growth of cell processes in differentiating NSCs. Therefore, both CaM and actin may jointly participate in the development and maturation of neurites, and this provides a theoretical basis for further study of the biological features of neuron-oriented NSC differentiation. IntroductionAs a multi-functional receptor of intercellular Ca . CaM is extensively localized in almost all tissues of vertebrates, plants and prokaryotes. This protein is especially rich in the brain and some endocrine organs (1). CaM has been shown to play different roles in different tissues and cells, under different physiological conditions or at different developmental stages. In addition, actin is a ubiquitous cytoskeletal protein, which is mainly involved in the formation of microfilaments and maintains normal cellular functions with the assistance of intermediate filaments and microtubules (2-4). As a cytoskeletal protein, actin plays an important role in cell growth and development, which not only closely correlates with cell morphology, but also participates in multiple functions such as cell movement, substance transport, as well as cell division, differentiation and gene expression (3,5).It has been shown that alteration of the intracellular Ca 2+ concentration is closely related to the function of actin (6). Therefore, CaM, a Ca 2+ receptor should also affect the function of actin (7). However, it is not clear whether this correlation exists in the directed differentiation of rat cerebral cortical neural stem cells (NSCs) into neurons. In this study, immunohistochemistry, RT-PCR and image analysis technology were conducted to detect the spatial expression of CaM and its action during the process of rat neuron-oriented cerebral cortical NSC differentiation. Immunofluorescence dual-labeling technology was used to label CaM and actin. Confocal ...

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Nestin expression in repopulating mesangial cells promotes their proliferation

Cited by 58 publications

References 44 publications

Transgelin is a marker of repopulating mesangial cells after injury and promotes their proliferation and migration

Transgelin is a marker of repopulating mesangial cells after injury and promotes their proliferation and migration

Nestin upregulation characterizes vascular remodeling secondary to hypertension in the rat

Involvement of calmodulin and actin in directed differentiation of rat cortical neural stem cells into neurons

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