Human β-cell regeneration

Jurczyk, Agata; Bortell, Rita; Alonso, Laura

doi:10.1097/med.0000000000000042

Cited by 13 publications

(7 citation statements)

References 95 publications

(101 reference statements)

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“…The findings of this study were in line with Jurczyk et al [26] who found that the histological studies on human tissue in adult who exposed to any stress factors showed insulin-expressing cells in ducts, isolated β-cells in the pancreatic parenchyma, and small islet clusters. PRP had consistently shown to potentiate stem cell proliferation, migration, and differentiation (Masoudi et al [33]).…”

Section: Discussionsupporting

confidence: 81%

“…Another one of PRP GFs; insulin growth factor, localized to the focal areas of regeneration and may play an important role in pancreatic regeneration by autocrine mechanisms through stimulation of DNA synthesis [35]. This could take place by using replication of already differentiated β-cells (β-cell plasticity) or neogenesis from putative islet stem cells in the ductal or acinar epithelium [26].…”

Section: Discussionmentioning

confidence: 99%

“…Numerous cells were functioning cells as the anti-insulin positive cells; β-cells, represented the major cell population of the islets. Hyperplastic and proliferative changes occurred in pancreas under the effect of certain stressors or stimuli led to formation of recent β-cells (Jurczyk et al [26]). Therefore, this study suggested that GFs of the PRP might act as stimuli for proliferation of these cells that led to an increase in β-cells number.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Platelet Rich Plasma (PRP) Injection on the Endocrine Pancreas of the Experimentally Induced Diabetes in Male Albino Rats: A Histological and Immunohistochemical Study

El‐Tahawy¹,

Rifaai²,

Saber³

et al. 2017

J Diabetes Metab

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Introduction: Diabetes mellitus is a global problem and several restoration approaches have been developed to induce beta (β) cells regeneration. Platelet rich plasma (PRP) is an autogenous and economical source of growth factors which nowadays used in the tissue repair. Aim:To test the hypothesis that PRP could play a role in the improvement of the structural changes occurred in the endocrine pancreas of experimentally-induced diabetic rats and the possible mechanisms through which PRP induced its effects to shed a light on the possible use of such application in the clinical field. Material and methods:Sixty male albino rats were used; 20 for obtaining the PRP and 40 were divided into 4 equal groups (10 rats each): control, PRP-group, diabetic group, PRP/diabetic group. Diabetes was induced by single intra-peritoneal injection of streptozotocin (50-60 mg/kg). The PRP was administered by SC injections in a dose of 0.5 mg/kg twice weekly for 3 weeks. Results:The diabetic group showed a significant increase in blood glucose levels compared to the control. Treatment with PRP significantly reduced the blood glucose levels compared to the diabetic group. The diabetic group showed variable marked morphological changes which diminished by the PRP administration. PRP/diabetic group had a significant increase in the mean number of pancreatic islets and β-cells/islet compared to the diabetic group. The islet cells appeared normal with scarcely seen vacuolations. The duct system showed several changes; stratifications, invagination of the surface epithelium to the underlying connective tissue, and sprouting of the ductal epithelial cells in between the lobules. Numerous small islets were noticed in a close association with the intralobular ducts. Small newly lobules with abundant connective tissue were organized. There were significant increases in the insulin immunopositive β-cells and PCNA positive cells in PRP/diabetic group compared to diabetic group. Conclusion:This study provides an evidence of the diabetic pancreatic islet regeneration in response to PRP treatment. The PRP stimulated islet cell regeneration and stimulated the induction of other sources of β-cells generation as the exocrine portion of the pancreas; ductal and acinar cells. In addition, PRP might put the pancreas into an environment similar to the postnatal developmental one where new lobules were formed. These will pave the future for a novel treatment for diabetes.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effect of Platelet Rich Plasma (PRP) Injection on the Endocrine Pancreas of the Experimentally Induced Diabetes in Male Albino Rats: A Histological and Immunohistochemical Study

El‐Tahawy¹,

Rifaai²,

Saber³

et al. 2017

J Diabetes Metab

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“…The increase in the size of the islets and budding of new islets by R-Tf-D-LP4 peptide treatment of STZ/HFD-32 fed mice raised the question as to the source of these β-cells. The possibility that they might regenerate is controversial and is currently a subject of debate [62,63]. One leading theory suggests that the formation of new islets is caused by the differentiation of progenitor or stem cells to β-cells [64], while an opposing theory suggests that differentiated cells in the pancreas or liver undergo a process of trans-differentiation by which cells de-differentiate and then re-differentiate to β-cells [63,65].…”

Section: Discussionmentioning

confidence: 99%

“…The possibility that they might regenerate is controversial and is currently a subject of debate [62,63]. One leading theory suggests that the formation of new islets is caused by the differentiation of progenitor or stem cells to β-cells [64], while an opposing theory suggests that differentiated cells in the pancreas or liver undergo a process of trans-differentiation by which cells de-differentiate and then re-differentiate to β-cells [63,65]. Another possible explanation is proliferation of β-cells, although the total β-cell proliferation rate was observed to be low in both mice and humans, as only a fraction of these cells proliferate [66].…”

Section: Discussionmentioning

confidence: 99%

The VDAC1-based R-Tf-D-LP4 Peptide as a Potential Treatment for Diabetes Mellitus

Pittala

Levy

et al. 2020

Cells

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Diabetes mellitus is a metabolic disorder approaching epidemic proportions. Non-alcoholic fatty liver disease (NAFLD) regularly coexists with metabolic disorders, including type 2 diabetes, obesity, and cardiovascular disease. Recently, we demonstrated that the voltage-dependent anion channel 1 (VDAC1) is involved in NAFLD. VDAC1 is an outer mitochondria membrane protein that serves as a mitochondrial gatekeeper, controlling metabolic and energy homeostasis, as well as crosstalk between the mitochondria and the rest of the cell. It is also involved in mitochondria-mediated apoptosis. Here, we demonstrate that the VDAC1-based peptide, R-Tf-D-LP4, affects several parameters of a NAFLD mouse model in which administration of streptozotocin (STZ) and high-fat diet 32 (STZ/HFD-32) led to both type 2 diabetes (T2D) and NAFLD phenotypes. We focused on diabetes, showing that R-Tf-D-LP4 peptide treatment of STZ/HFD-32 fed mice restored the elevated blood glucose back to close to normal levels, and increased the number and average size of islets and their insulin content as compared to untreated controls. Similar results were obtained when staining the islets for glucose transporter type 2. In addition, the R-Tf-D-LP4 peptide decreased the elevated glucose levels in a mouse displaying obese, diabetic, and metabolic symptoms due to a mutation in the obese (ob) gene. To explore the cause of the peptide-induced improvement in the endocrine pancreas phenotype, we analyzed the expression levels of the proliferation marker, Ki-67, and found it to be increased in the islets of STZ/HFD-32 fed mice treated with the R-Tf-D-LP4 peptide. Moreover, peptide treatment of STZ/HFD-32 fed mice caused an increase in the expression of β-cell maturation and differentiation PDX1 transcription factor that enhances the expression of the insulin-encoding gene, and is essential for islet development, function, proliferation, and maintenance of glucose homeostasis in the pancreas. This increase occurred mainly in the β-cells, suggesting that the source of their increased number after R-Tf-D-LP4 peptide treatment was most likely due to β-cell proliferation. These results suggest that the VDAC1-based R-Tf-D-LP4 peptide has potential as a treatment for diabetes.

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Stem and progenitor cells of the mammalian olfactory epithelium: Taking poietic license

Schwob

Jang

Holbrook

et al. 2016

J of Comparative Neurology

214

238

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The capacity of the olfactory epithelium (OE) for lifelong neurogenesis and regeneration depends on the persistence of neurocompetent stem cells, which self-renew as well as generating all of the cell types found within the nasal epithelium. This Review focuses on the types of stem and progenitor cells in the epithelium and their regulation. Both horizontal basal cells (HBCs) and some among the population of globose basal cells (GBCs) are stem cells, but the two types plays vastly different roles. The GBC population includes the basal cells that proliferate in the uninjured OE and is heterogeneous with respect to transcription factor expression. From upstream in the hierarchy to downstream, GBCs encompass 1) Sox2+/Pax6+ stem-like cells that are totipotent and self-renew over the long term, 2) Ascl1+ transit-amplifying progenitors with a limited capacity for expansive proliferation, and 3) Neurog1+/NeuroD1+ immediate precursor cells that make neurons directly. In contrast, the normally quiescent HBCs are activated to multipotency and proliferate when sustentacular cells are killed, but not when only OSNs die, indicating that HBCs are reserve stem cells that respond to severe epithelial injury. The master regulator of HBC activation is the ΔN isoform of the transcription factor p63; eliminating ΔNp63 unleashes HBC multipotency. Notch signaling, via Jagged1 ligand on Sus cells and Notch1 and Notch2 receptors on HBCs, is likely to play a major role in setting the level of p63 expression. Thus, ΔNp63 becomes a potential therapeutic target for reversing the neurogenic exhaustion characteristic of the aged OE.

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Human β-cell regeneration

Cited by 13 publications

References 95 publications

Effect of Platelet Rich Plasma (PRP) Injection on the Endocrine Pancreas of the Experimentally Induced Diabetes in Male Albino Rats: A Histological and Immunohistochemical Study

Effect of Platelet Rich Plasma (PRP) Injection on the Endocrine Pancreas of the Experimentally Induced Diabetes in Male Albino Rats: A Histological and Immunohistochemical Study

The VDAC1-based R-Tf-D-LP4 Peptide as a Potential Treatment for Diabetes Mellitus

Stem and progenitor cells of the mammalian olfactory epithelium: Taking poietic license

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