Isolation and characterization of human islet stellate cells

Zha, Min; Xu, Wei; Jones, Peter M.; Sun, Zilin

doi:10.1016/j.yexcr.2015.11.002

Cited by 29 publications

(30 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our previous studies have confirmed the presence of stellate cells within the islets (ISCs), which are identical in the expression of retinoid-containing fat droplets [51,52,53,54,55]. A loss of oil red O-stained fat droplets was associated with the activation of diabetic ISCs, and we speculate whether the transfer of lipid droplets from the inside to the outside of the ISCs leads to local fat deposition and the inhibition of normal β-cell function.…”

Section: Discussionsupporting

confidence: 67%

Pancreatic Fat is not significantly correlated with β-cell Dysfunction in Patients with new-onset Type 2 Diabetes Mellitus using quantitative Computed Tomography

Sang

Sun

et al. 2020

Int. J. Med. Sci.

Self Cite

View full text Add to dashboard Cite

Objective: Type 2 diabetes mellitus (T2DM) is a chronic condition resulting from insulin resistance and insufficient β-cell secretion, leading to improper glycaemic regulation. Previous studies have found that excessive fat deposits in organs such as the liver and muscle can cause insulin resistance through lipotoxicity that affects β-cell function. The relationships between fat deposits in pancreatic tissue, the function of β-cells, the method of visceral fat evaluation and T2DM have been sought by researchers. This study aims to elucidate the role of pancreatic fat deposits in the development of T2DM using quantitative computed tomography (QCT), especially their effects on islet β-cell function. Methods: We examined 106 subjects at the onset of T2DM who had undergone abdominal QCT. Estimated pancreatic fat and liver fat were quantified using QCT and calculated. We analysed the correlations with Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) scores and other oral glucose tolerance test-derived parameters that reflect islet function. Furthermore, correlations of estimated pancreatic fat and liver fat with the area under the curve for insulin (AUCINS) and HOMA-IR were assessed with partial correlation analysis and demonstrated by scatter plots. Results: Associations were found between estimated liver fat and HOMA-IR, AUCINS, the modified β-cell function index (MBCI) and Homeostatic Model Assessment β (HOMA-β). However, no significant differences existed between estimated pancreas fat and those parameters. Similarly, after adjustment for sex, age and body mass index, only estimated liver fat was correlated with HOMA-IR and AUCINS. Conclusions: This study suggests no significant correlation between pancreatic fat deposition and β-cell dysfunction in the early stages of T2DM using QCT as a screening tool. The deposits of fat in the pancreas and the resulting lipotoxicity may play an important role in the late stage of islet cell function dysfunction as the course of T2DM progresses.

show abstract

Section: Discussionsupporting

confidence: 67%

Pancreatic Fat is not significantly correlated with β-cell Dysfunction in Patients with new-onset Type 2 Diabetes Mellitus using quantitative Computed Tomography

Sang

Sun

et al. 2020

Int. J. Med. Sci.

Self Cite

View full text Add to dashboard Cite

show abstract

“…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

Self Cite

View full text Add to dashboard Cite

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.

show abstract

“…But their proliferation and migration rates were significantly lower than typical PSCs. Recently, Zha et al (2016) used standard explants techniques to isolate the corresponding ISCs in human pancreatic tissue, which were also different from the typical PSCs. Human ISCs express α-SMA, desmin, vimentin and GFAP, as well as collagen I, collagen III and fibronectin.…”

Section: Islet Stellate Cells (Iscs)mentioning

confidence: 99%

“…Islet stellate cells can act as subgroups of PSCs and interact with pancreatic β-cells, included enhancing β-cell apoptosis, inhibiting proliferation, and decreasing β-cell function, which are important in islet fibrosis and islet cell dysfunction ( Li et al, 2016 ; Zha et al, 2016 ).…”

Section: Islet Stellate Cells (Iscs)mentioning

confidence: 99%

A Rising Star in Pancreatic Diseases: Pancreatic Stellate Cells

et al. 2018

View full text Add to dashboard Cite

Pancreatic stellate cell (PSC) is a type of pluripotent cell located between pancreatic lobules and the surrounding area of acinars. When activated, PSC can be transformed into myofibroblast-like cell. A number of evidences suggest that activated PSC is the main source of the accumulation of extracellular matrix (ECM) protein under the pathological conditions, which lead to pancreatic fibrosis in chronic pancreatitis and pancreatic cancer. Recent studies have found that PSC also plays an important role in the endocrine cell function, islet fibrosis and diabetes. In order to provide new strategies for the treatment of pancreatic diseases, this paper systematically summarizes the recent researches about the biological behaviors of PSC, including its stem/progenitor cell characteristics, secreted exosomes, cellular senescence, epithelial mesenchymal transformation (EMT), energy metabolism and direct mechanical reprogramming.

show abstract

Isolation and characterization of human islet stellate cells

Abstract: Similar to our previous rat experiment, the current study shows that human islets also contain ISC which is phenotypically similar but not identical to human PSC.

Cited by 29 publications

References 38 publications

Pancreatic Fat is not significantly correlated with β-cell Dysfunction in Patients with new-onset Type 2 Diabetes Mellitus using quantitative Computed Tomography

Pancreatic Fat is not significantly correlated with β-cell Dysfunction in Patients with new-onset Type 2 Diabetes Mellitus using quantitative Computed Tomography

Islet Stellate Cells Regulate Insulin Secretion via Wnt5a in Min6 Cells

A Rising Star in Pancreatic Diseases: Pancreatic Stellate Cells

Contact Info

Product

Resources

About