scholarly journals In vitro studies of the stimulation of insulin secretion and B-cell proliferation by rat placental lactogen-II during pregnancy in rats

Reproduction ◽  
1997 ◽  
Vol 109 (1) ◽  
pp. 145-152 ◽  
Author(s):  
M. Kawai ◽  
K. Kishi
Keyword(s):  
Cell Proliferation ◽  
Insulin Secretion ◽  
B Cell ◽  
In Vitro Studies ◽  
Placental Lactogen ◽  
Stimulation Of

scholarly journals IN VITRO STIMULATION OF B-CELL INDUCES DIFFERENTIATION AND NOT PROLIFERATION

1989 ◽  
Vol 72 (1) ◽  
pp. 113-113 ◽  
Author(s):  
David Barnett ◽  
Jackie Storr ◽  
George A. Buckley ◽  
John T. Reilly
Keyword(s):  
B Cell ◽  
Stimulation Of

Direct effect of parathyroid hormone on insulin secretion from pancreatic islets

1990 ◽  
Vol 258 (6) ◽  
pp. E975-E984 ◽  
Author(s):  
G. Z. Fadda ◽  
M. Akmal ◽  
L. G. Lipson ◽  
S. G. Massry
Keyword(s):  
Insulin Secretion ◽  
Parathyroid Hormone ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Direct Effect ◽  
Indirect Evidence ◽  
Cytosolic Calcium ◽  
Dependent Manner ◽  
Stimulation Of

Indirect evidence indicates that parathyroid hormone (PTH) interacts with pancreatic islets and modulates their insulin secretion. This property of PTH has been implicated in the genesis of impaired insulin release in chronic renal failure. We examined the direct effect of PTH-(1-84) and PTH-(1-34) on insulin release using in vitro static incubation and dynamic perifusion of pancreatic islets from normal rats. Both moieties of the hormone stimulated in a dose-dependent manner glucose-induced insulin release but higher doses inhibited glucose-induced insulin release. This action of PTH was modulated by the calcium concentration in the media. The stimulatory effect of PTH was abolished by its inactivation and blocked by its antagonist [Tyr-34]bPTH-(7-34)NH2. PTH also augmented phorbol ester (TPA)-induced insulin release, stimulated adenosine 3',5'-cyclic monophosphate (cAMP) generation by pancreatic islets, and significantly increased (+50 +/- 2.7%, P less than 0.01) their cytosolic calcium. Verapamil inhibited the stimulatory effect of PTH on insulin release. The data show that 1) pancreatic islets are a PTH target and may have PTH receptors, 2) stimulation of glucose-induced insulin release by PTH is mediated by a rise in cytosolic calcium, 3) stimulation of cAMP production by PTH and a potential indirect activation of protein kinase C by PTH may also contribute to the stimulatory effect on glucose-induced insulin release, and 4) this action of PTH requires calcium in incubation or perifusion media.

scholarly journals Effect of platelet-rich fibrin on cell proliferation, migration, differentiation, inflammation, and osteoclastogenesis: a systematic review of in vitro studies

2019 ◽  
Vol 24 (2) ◽  
pp. 569-584 ◽  
Author(s):  
Franz-Josef Strauss ◽  
Jila Nasirzade ◽  
Zahra Kargarpoor ◽  
Alexandra Stähli ◽  
Reinhard Gruber
Keyword(s):  
Systematic Review ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Bone Regeneration ◽  
Therapeutic Potential ◽  
In Vitro Studies ◽  
Bioactive Molecules ◽  
Platelet Rich Fibrin ◽  
Regenerative Dentistry

Abstract Objective To systematically assess the effects of platelet-rich fibrin (PRF) on in vitro cellular behavior. Methods A systematic electronic search using MEDLINE database was performed. In vitro studies using PRF were considered and articles published up to June 31, 2018 were screened. Eligible studies were selected based on the use of human PRF. Results In total, 1746 titles were identified with the search terms, from these 37 met the inclusion criteria and were chosen for data extraction. In addition, 16 new studies, mainly published in 2019, were also included in the analysis resulting in 53 studies. No meta-analysis could be performed due to the heterogeneity of study designs. Included studies show that PRF enhances proliferation, migration, adhesion, and osteogenic differentiation on a variety of cell types along with cell signaling activation. Furthermore, PRF reduces inflammation, suppresses osteoclastogenesis, and increases the expression of various growth factors in mesenchymal cells. Summary and conclusions Despite some notable differences of the studies, the overall findings suggest a positive effect of PRF on cell proliferation, migration, adhesion, differentiation, and inflammation pointing towards a therapeutic potential in regenerative dentistry. Clinical relevance PRF serves as a reservoir of bioactive molecules to support wound healing and bone regeneration. Although the cellular mechanisms by which PRF supports the clinical outcomes remain unclear, in vitro research provides possible explanations. This systematic review aims to provide an update of the existing research on how PRF affects basic physiological processes in vitro. The overall findings suggest that PRF induces cell proliferation, migration, adhesion, and differentiation along with possessing anti-inflammatory properties further supporting its therapeutic potential in wound healing and bone regeneration.

scholarly journals miR-29a Negatively Affects Glucose-Stimulated Insulin Secretion and MIN6 Cell Proliferation via Cdc42/β-Catenin Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-13
Author(s):  
Jing Duan ◽  
Xian-Ling Qian ◽  
Jun Li ◽  
Xing-Hua Xiao ◽  
Xiang-Tong Lu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Insulin Secretion ◽  
High Glucose ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Glucose Stimulation ◽  
Inhibition Of Proliferation ◽  
Glucose Stimulated Insulin Secretion

Background. Diabetes is a progressive metabolic disease characterized by hyperglycemia. Functional impairment of islet β cells can occur to varying degrees. This impairment can initially be compensated for by proliferation and metabolic changes of β cells. Cell division control protein 42 (Cdc42) and the microRNA (miRNA) miR-29 have important roles in β-cell proliferation and glucose-stimulated insulin secretion (GSIS), which we further explored using the mouse insulinoma cell line MIN6. Methods. Upregulation and downregulation of miR-29a and Cdc42 were accomplished using transient transfection. miR-29a and Cdc42 expression was detected by real-time PCR and western blotting. MIN6 proliferation was detected using a cell counting kit assay. GSIS under high-glucose (20.0 mM) or basal-glucose (5.0 mM) stimulation was detected by enzyme-linked immunosorbent assay. The miR-29a binding site in the Cdc42 mRNA 3′-untranslated region (UTR) was determined using bioinformatics and luciferase reporter assays. Results. miR-29a overexpression inhibited proliferation (P<0.01) and GSIS under high-glucose stimulation (P<0.01). Cdc42 overexpression promoted proliferation (P<0.05) and GSIS under high-glucose stimulation (P<0.05). miR-29a overexpression decreased Cdc42 expression (P<0.01), whereas miR-29a downregulation increased Cdc42 expression (P<0.01). The results showed that the Cdc42 mRNA 3′-UTR is a direct target of miR-29a in vitro. Additionally, Cdc42 reversed miR-29a-mediated inhibition of proliferation and GSIS (P<0.01). Furthermore, miR-29a inhibited β-catenin expression (P<0.01), whereas Cdc42 promoted β-catenin expression (P<0.01). Conclusion. By negatively regulating Cdc42 and the downstream molecule β-catenin, miR-29a inhibits MIN6 proliferation and insulin secretion.

HUMAN PANCREATIC B-CELL PROLIFERATION IN VITRO AND IN VIVO

1996 ◽  
Vol 24 (4) ◽  
pp. 511S-511S
Author(s):  
B. Tyrberg ◽  
D.L. Eizirik ◽  
C. Hellerström ◽  
D.G. Pipeleers ◽  
A. Andersson
Keyword(s):  
Cell Proliferation ◽  
B Cell ◽  
Pancreatic B Cell ◽  
Proliferation In Vitro

Effect of gestational hyperglycemia on insulin secretion in vivo and in vitro by fetal rat pancreas

1986 ◽  
Vol 251 (1) ◽  
pp. E86-E91 ◽  
Author(s):  
M. T. Bihoreau ◽  
A. Ktorza ◽  
A. Kervran ◽  
L. Picon
Keyword(s):  
Insulin Secretion ◽  
B Cell ◽  
Insulin Release ◽  
Plasma Insulin ◽  
Cell Function ◽  
Pregnant Rats ◽  
Fetal Rat ◽  
Gestational Hyperglycemia

The effects of gestational hyperglycemia on B-cell function were studied in near-term fetuses from unrestrained pregnant rats made slightly or highly hyperglycemic using continuous glucose infusion during the last week of pregnancy. Pancreatic and plasma insulin and insulin secretion in vitro were studied in the fetuses. Compared with controls, slightly hyperglycemic fetuses showed increased pancreatic and plasma insulin concentrations and similar insulin release in response to glucose in vitro. In highly hyperglycemic fetuses, pancreatic and plasma insulin concentrations were unchanged compared with controls, and insulin release in vitro was insensitive to glucose and to the mixture glucose plus theophylline. These results confirm that glucose is able to stimulate insulin secretion in normal or slightly hyperglycemic fetuses and suggest that severe hyperglycemia per se, without association of other metabolic disorders or toxic injuries, profoundly alters the stimulus-secretion coupling of the fetal rat B-cell.

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