Isolation and characterization of islet stellate cells in rat

Zha, Min; Li, Fengfei; Xu, Wei; Chen, Bijun; Sun, Zilin

doi:10.4161/isl.28701

Cited by 45 publications

(51 citation statements)

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“…Furthermore, as it has been also described for other developing organs, mesothelial‐derived cells contribute to an organ‐specific cell type, the pancreatic stellate cells, including the subtype known as islet stellate cells (Zha et al, ). This contribution is significant, accounting for more than a half of the PSC by midgestation.…”

Section: Discussionmentioning

confidence: 81%

Role of the Wilms' tumor suppressor gene Wt1 in pancreatic development

Ariza

Cañete

Rojas

et al. 2018

Developmental Dynamics

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The Wilms tumor suppressor gene (Wt1) encodes a transcription factor involved in the development of a number of organs, but the role played by Wt1 in pancreatic development is unknown. The pancreas contains a population of pancreatic stellate cells (PSC) very important for pancreatic physiology. We described elsewhere that hepatic stellate cells originate from the WT1-expressing liver mesothelium. Thus, we checked if the origin of PSCs was similar. WT1 expression is restricted to the pancreatic mesothelium. Between embryonic day (E) 10.5 and E15.5, this mesothelium gives rise to mesenchymal cells that contribute to a major part of the PSC and other cell types including endothelial cells. Most WT1 systemic mutants show abnormal localization of the dorsal pancreas within the mesentery and intestinal malrotation by E14.0. Embryos with conditional deletion of WT1 between E9.5 and E12.5 showed normal dorsal pancreatic bud and intestine, but the number of acini in the ventral bud was reduced approximately 30% by E16.5. Proliferation of acinar cells was reduced in WT1 systemic mutants, but pancreatic differentiation was not impaired. Thus, mesothelial-derived cells constitute an important subpopulation of pancreatic mesodermal cells. WT1 expression is not essential for pancreas development, although it influences intestinal rotation and correct localization of the dorsal pancreas within the mesogastrium. Developmental Dynamics 247:924-933, 2018. © 2018 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 81%

Role of the Wilms' tumor suppressor gene Wt1 in pancreatic development

Ariza

Cañete

Rojas

et al. 2018

Developmental Dynamics

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“…We found that insulin secretion from islets cocultured in vitro with db/m mouse ISCs was significantly increased compared to that from islets cocultured with ISCs from db/db mice. Subsequent iTRAQ protein screening of the ISCs showed that both ISCs cultured under static conditions and their supernatants showed high Wnt5a protein expression compared with diabetic ISCs [24][25][26][27][28][29][30]. e mechanisms leading to ISCs quiescence play an important role in regulating islet function via the Wnt5a-Fzd5 system and can help us understand the crosstalk between cells inside the islets of Langerhans and serve as a target for the prevention of diabetes.…”

Section: Discussionmentioning

confidence: 99%

Islet Stellate Cells Regulate Insulin Secretion via Wnt5a in Min6 Cells

Jones

Geng

et al. 2020

International Journal of Endocrinology

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Background. Type 2 diabetes mellitus is a serious public health problem worldwide. Accumulating evidence has shown that β-cell dysfunction is an important mechanism underlying diabetes mellitus. e changes in the physiological state of islet stellate cells (ISCs) and the effects of these cells on β cell function play an important role in the development of diabetes. is study aimed at elucidating the mechanism by which ISCs regulate insulin secretion from Min6 cells via the Wnt5a protein. Methods. Glucosestimulated insulin secretion (GSIS) from Min6 cells was examined by estimating the insulin levels in response to high glucose challenge after culture with ISC supernatant or exogenous Wnt5a. Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) analyses were used to observe changes in the β-catenin, receptor tyrosine kinase-like orphan receptor 2 (Ror2), Ca (2+)/calmodulin (CaM)-dependent protein kinase II (CamKII), forkhead box O1 (FoxO1), pancreatic and duodenal homeobox 1 (PDX1), glucose transporter 2 (Glut2), insulin, and Cask mRNA and protein levels in the Wnt and insulin secretory pathways. Flow cytometry was used to confirm the intracellular Ca 2+ concentration in Min6 cells. Results. We observed a significant increase in insulin secretion from Min6 cells cocultured in vitro with supernatant from db/m mouse ISCs compared to that from Min6 cells cocultured with supernatant from db/db mouse ISCs; e intracellular Ca 2+ concentration in Min6 cells increased in cultured in vitro with supernatant from db/m mouse ISCs and exogenous Wnt5a compared to that from control Min6 cells. Culture of Min6 cells with exogenous Wnt5a caused a significant increase in pCamKII, pFoxO1, PDX-1, and Glut2 levels compared to those in Min6 cells cultured alone; this treatment further decreased Ror2 and Cask expression but did not affect β-catenin expression. Conclusion. ISCs regulate insulin secretion from Min6 cells through the Wnt5a protein-induced Wntcalcium and FoxO1-PDX1-GLUT2-insulin signalling cascades.

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“…In our previous rat research, using explant techniques, we isolated ISC exhibiting similar appearance to classical PSC from fresh isolated rat islets [20]. And immunofluorescent staining showed these out-growing cells were negative for insulin, so we excluded the possibility of -cell out-growth.…”

Section: Discussionmentioning

confidence: 99%

“…However, we have reported that using standard explants techniques, we isolated rat islet stellate cell (ISC) from endocrine pancreatic islets [20]. Compared with rat PSC, ISC is more rapidly activated than PSC in vitro.…”

Section: Introductionmentioning

confidence: 99%