Nestin Is Expressed in Vascular Endothelial Cells in the Adult Human Pancreas

Klein, Tino; Ling, Zhidong; Heimberg, Harry; Madsen, Ole; Heller, R. Scott; Serup, Palle

doi:10.1177/002215540305100601

Cited by 99 publications

(80 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4F,G) and of PC2 Ϫ/Ϫ , PC2 ϩ/ϩ , and Gcgr Ϫ/Ϫ mice (not shown) contained nestin ϩ cells that did not express hormones. These cells are likely to be the mesenchymal nestin ϩ cells described by others (Delacour et al, 2004;Esni et al, 2004;Humphrey et al, 2003;Klein et al, 2003;Lardon et al, 2002;Treutelaar et al, 2003).…”

Section: Reappearance Of Nestin Expression In Pancreatic Cells Of Adumentioning

confidence: 69%

“…This possibility was supported by the discovery of nestin ϩ cells in epithelial cells of the pancreatic bud of mouse embryos from e-10 to e-15 (Esni et al, 2004), raising the prospect that these cells were endocrine precursor cells. This possibility is controversial since several reports indicated that nestin expression was restricted to cells derived from the mesenchyme (Humphrey et al, 2003;Klein et al, 2003;Lardon et al, 2002;Selander and Edlund, 2002;Treutelaar et al, 2003). The derivation of pancreatic endocrine and exocrine cells from nestin precursors is further complicated by conflicting results obtained from cell lineage analysis of pancreatic cells using molecular marking techniques.…”

Section: Introductionmentioning

confidence: 99%

“…Nestin was used as a marker to isolate a subpopulation of embryonic stem cells with the ability to initiate insulin expression in vitro (Blyszczuk et al, 2003;Lumelsky et al, 2001). Moreover, islets of adult mice and rats were found to contain nestin ϩ cells (Hunziker and Stein, 2000;Zulewski et al, 2001) and these cells were reported to differentiate into endocrine and exocrine cells in culture (Abraham et al, 2004;Hunziker and Stein, 2000;Klein et al, 2003;Seaberg et al, 2004;Zulewski et al, 2001). These observations suggest that embryonic islet precursor cells express nestin but that its expression in vivo is down-regulated and becomes undetectable during the initiation of endocrine differentiation.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Nestin expression in pancreatic endocrine and exocrine cells of mice lacking glucagon signaling

Kedees¹,

Guz²,

Vuguin³

et al. 2007

Developmental Dynamics

View full text Add to dashboard Cite

Nestin, a marker of neural stem cells, is also expressed by cells located in the epithelium of the pancreatic primordium and by a subpopulation of exocrine cells but not by endocrine cells. These findings raised the possibility that the pancreatic epithelium is heterogeneous and comprised of subpopulations of exocrine/ nestin-positive and endocrine/nestin-negative precursor cells. We examined this issue in two mutant mouse models characterized by protracted expression of several embryonal properties in islet cells. One mutant line comprises mice lacking mature glucagon due to abrogation of proprotein convertase-2 (PC2 ؊/؊ ), responsible for the conversion of proglucagon into glucagon, while the second line consists of mice with a global deletion of the glucagon receptor (Gcgr ؊/؊ ). We demonstrate that nestin is transiently expressed by acinar cells and by insulin and glucagon cells of islets of both lines of mice. In addition, the lack of glucagon signaling increased nestin mRNA levels in pancreas of mutant embryos and adult mice. We conclude that nestin؉ cells located in the pancreatic primordium generate the cells of the endocrine and exocrine lineages. Furthermore, our results suggest that nestin expression is regulated by glucagon signaling.

show abstract

Section: Reappearance Of Nestin Expression In Pancreatic Cells Of Adumentioning

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Nestin expression in pancreatic endocrine and exocrine cells of mice lacking glucagon signaling

Kedees¹,

Guz²,

Vuguin³

et al. 2007

Developmental Dynamics

View full text Add to dashboard Cite

show abstract

“…Nestin expression did not seem to predict the identity of these cells, but all of the colonies derived from these cells expressed nestin and did not co-express endothelial and epithelial cell markers. Based on these findings, the authors suggested the existence of a different nestin-positive progenitor cell other than those pancreatic epithelial cell progenitors previously described in vivo (Esni et al 2004, Klein et al 2003, Selander & Edlund 2002. It still remains to be elucidated whether different populations of nestin-positive cells committed to different cell fates exist in different stages of pancreatic development.…”

Section: Days In Culturementioning

confidence: 89%

Co-localization of nestin and insulin and expression of islet cell markers in long-term human pancreatic nestin-positive cell cultures

Maria‐Engler

Corrêa-Giannella²,

Labriola³

et al. 2004

Journal of Endocrinology

View full text Add to dashboard Cite

Strategies to differentiate progenitor cells into cells in vitro have been considered as an alternative to increase cell availability prior to transplantation. It has recently been suggested that nestin-positive cells could be multipotential stem cells capable of expressing endocrine markers upon specific stimulation; however, this issue still remains controversial. Here, we characterized short-and longterm islet cell cultures derived from three different human islet preparations, with respect to expression of nestin and islet cell markers, using confocal microscopy and semiquantitative RT-PCR. The number of nestin-positive cells was found to be strikingly high in long-term cultures. In addition, a large proportion (49·7%) of these nestinpositive cells, present in long-term culture, are shown to be proliferative, as judged by BrdU incorporation. The proportion of insulin-positive cells was found to be high in short-term (up to 28 days) cultures and declined thereafter, when cells were maintained in the presence of 10% serum, concomitantly with the decrease in insulin and PDX-1 expression. Interestingly, insulin and nestin co-expression was observed as a rare event in a small proportion of cells present in freshly isolated human islets as well as in purified islet cells cultured in vitro for long periods of time. In addition, upon long-term subculturing of nestin-positive cells in 10% serum, we observed reappearance of insulin expression at the mRNA level; when these cultures were shifted to 1% serum for a month, expression of insulin, glucagon and somatostatin was also detected, indicating that manipulating the culture conditions can be used to modulate the nestin-positive cell's fate. Attempts to induce cell differentiation by plating nestin-positive cells onto Matrigel revealed that these cells tend to aggregate to form islet-like clusters, but this is not sufficient to increase insulin expression upon shortterm culture. Our data corroborate previous findings indicating that, at least in vitro, nestin-positive cells may undergo the early stages of differentiation to an islet cell phenotype and that long-term cultures of nestin-positive human islet cells may be considered as a potential source of precursor cells to generate fully differentiated/ functional cells.

show abstract

“…18,19,40) Previous observation suggested that testis Nestin + cells also express GATA-4 that involved in embryogenesis and myocardial differentiation and function maintenance. 16,41) Similar to other organs, we have found that Nestin also exists in the myocardium and up-regulates early in DCM mice, which might be associated with inhibiting cardiomyocyte depletion.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Nestin<sup>+</sup> Cells Derived from Early Stage of Dilated Cardiomyopathy Enhanced the Survival of the Doxorubicin-Injured Cardiac Muscle HL-1 Cells

Xie

Liao

et al. 2018

Int. Heart J.

View full text Add to dashboard Cite

SummaryDilated cardiomyopathy (DCM), as one of the common cardiomyopathies, is a disease of the heart muscle; however, the etiology and pathogenesis of DCM were still poorly understood. Nestin has been reported a special marker of stem/progenitor cells in various tissues, and the tissue resident Nestin + cells could promote the wound healing and tissue remodeling. However, it remains unclear whether Nestin + cells participate in the protection of cardiomyocytes during the pathogenesis of DCM. Here the model of mice DCM was induced by doxorubicin (DOX) intraperitoneal injection and observed heart failure and ventricular enlargement via echocardiography and histologic analysis, respectively. During DCM pathogenesis, the number of Nestin + cells showed a significant peak on day 6 after DOX treatment, which then gradually decreases to lower than normal levels after day 30 in the total population of the heart. Furthermore, we found that the isolated increased heart-derived Nestin + cells are mesenchymal property and could protect DOX-induced HL-1 cells toxicity in vitro by promoting their proliferation and inhibiting their apoptosis. Collectively, our results showed that Nestin + cells increased during DCM pathogenesis and played an important role in protecting against the DOX-induced HL-1 cells loss via regulating proliferation and apoptosis. Thus, the loss of Nestin + cells might be an etiology to DCM pathogenesis, and these cells could be a promising candidate cell source for study and treatment of DCM patients.(Int Heart J 2018; 59: 180-189)

show abstract

Nestin Is Expressed in Vascular Endothelial Cells in the Adult Human Pancreas

Cited by 99 publications

References 48 publications

Nestin expression in pancreatic endocrine and exocrine cells of mice lacking glucagon signaling

Nestin expression in pancreatic endocrine and exocrine cells of mice lacking glucagon signaling

Co-localization of nestin and insulin and expression of islet cell markers in long-term human pancreatic nestin-positive cell cultures

Cardiac Nestin<sup>+</sup> Cells Derived from Early Stage of Dilated Cardiomyopathy Enhanced the Survival of the Doxorubicin-Injured Cardiac Muscle HL-1 Cells

Contact Info

Product

Resources

About