Streptozotocin-Induced Diabetic Rat–Derived Bone Marrow Mesenchymal Stem Cells Have Impaired Abilities in Proliferation, Paracrine, Antiapoptosis, and Myogenic Differentiation

Jin, Peifeng; Zhang, X.; Wu, Yuning; Li, L.; Yin, Qiushi; Zheng, Lei; Zhang, H.; Sun, Chengcao

doi:10.1016/j.transproceed.2010.05.145

Cited by 80 publications

(67 citation statements)

References 28 publications

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“…In this report, MSCs had impaired therapeutic transplant efficacy for myocardial infarction (MI) when obtained from old mice, and this was related to pigment epithelium-derived factor (PEDF). Previous studies have focused on the biological characteristics of MSCs in a rat model [14] and in patients with CHD [15]. Thus, aging may influence the efficacy of MSC transplantation [6,16], but at present the importance of MSC donor age on therapeutic efficacy is uncertain [17].…”

Section: Instructionmentioning

confidence: 99%

Advanced Age Impairs Cardioprotective Function of Mesenchymal Stem Cell Transplantation from Patients to Myocardially Infarcted Rats

Liu

Liu²,

Han³

et al. 2014

Cardiology

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Objectives: Mesenchymal stem cells (MSCs) have limited clinical therapeutic effects in older myocardial infarction (MI) patients. Thus, whether younger MSCs might confer greater protection is worth investigating. Methods: Human MSCs (hMSCs) were isolated before coronary artery bypass graft surgery and growth characteristics of hMSCs at passage 3 were observed. Vascular endothelial growth factor (VEGF) and Bcl-2 mRNA and protein expression from hMSCs were measured. In vivo, 45 adult male rats with MI were randomized to receive one of three treatments: old hMSCs, young hMSCs or culture medium (control) transplanted into infarcted myocardium. Echocardiography, TUNEL, immunohistochemistry and Western blot were used to assess results. Results: hMSC proliferation in the old group was significantly lower than the young group. VEGF decreased 35% and Bcl-2 decreased more than 60% at the mRNA level; VEGF and Bcl-2 protein were decreased in the old versus the young group. hMSC transplantation may improve cardiac function, but MSC source may affect therapeutic efficacy. Similar data were obtained from TUNEL, immunohistochemistry and Western blot. Conclusion: Transplantation of hMSCs improves heart function, but proliferative ability and myocardial protection decrease with older MSCs, likely due to differences between VEGF and Bcl-2 expression and reduced anti-apoptosis.

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Section: Instructionmentioning

confidence: 99%

Advanced Age Impairs Cardioprotective Function of Mesenchymal Stem Cell Transplantation from Patients to Myocardially Infarcted Rats

Liu

Liu²,

Han³

et al. 2014

Cardiology

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“…67,71 It is also known to reduce the proliferation, migration, and differentiation potential of periodontal ligament cells (PDLCs), 72,73 gingival fibroblasts (GFs), 74 and mesenchymal stem cells (MSCs). 75,76 Hyperglycemia also triggers a variety of collagen changes. One study showed reduced synthesis of both collagen and glycosaminoglycan in hyperglycemic culture conditions and fibroblasts from diabetic patients.…”

Section: Direct Effects Of Hyperglycemiamentioning

confidence: 99%

Interrelationships of periodontitis and diabetes: A review of the current literature

Chang

Lim

2012

Journal of Dental Sciences

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Diabetes and periodontitis are common chronic diseases in the world, and abundant epidemiological evidence implies a bidirectional relationship between the two diseases. It appears that diabetes is a risk factor for greater periodontal destruction, whereas managing periodontitis can also contribute to better glycemic control. The underlying regulatory mechanisms are also bidirectional. The hyperglycemic status may directly alter subgingival microbial compositions, impair cellular function, and change collagen metabolism. The formation of advanced glycation end-products (AGEs) can further modify the extracellular matrix, and establishment of cellular receptor binding can amplify inflammation. Moreover, periodontitis also induces hyperlipidemia and insulin resistance. This cyclical relationship converges via overproduction of proinflammatory cytokines, such as tumor necrosis factor-a and interleukin-1b. Thus, this article highlights the importance of maintaining periodontal health to eliminate systemic complications and meticulous metabolic control to prevent further periodontal destruction. From a systemic aspect, targeting proinflammatory cytokines or receptors of AGEs could be a potential modality for treating periodontitis.

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“…Previous studies (Jin et al, 2010;Ling et al, 2012;Zhang & Yan, 2013) have shown that there is a significant reduction in CEPC levels in STZ-induced diabetic rats. The discrepancies between our findings and these reports in the literature can be partly explained by the selection of the STZ dosage (55 mg/kg; 30 mg/kg; 50 mg/kg), the timing of its application (not indicated) and other unknown environmental factors.…”

Section: Discussionmentioning

confidence: 91%

“…Circulating endothelial progenitor cells mobilise to the sites of damaged tissue to induce vascular repair, but their recruitments are impaired by hyperglycaemia (Thangarajah et al, 2010). Chronic hyperglycaemia, as a result of Diabetes mellitus (DM), increases reactive oxygen species (ROS) levels leading to oxidative stress (King & Loeken, 2004), which in turn causes endothelial cell (EC) activation. This inflammatory and immunological response (Hunt & Jurd, 1998) is characterised by vascular endothelial hypertrophy and thickening, leading to permanent EC damage .…”

Section: Introductionmentioning

confidence: 99%

“…This inflammatory and immunological response (Hunt & Jurd, 1998) is characterised by vascular endothelial hypertrophy and thickening, leading to permanent EC damage . A number of studies (Liao et al, 2010;Chen et al, 2013;Liu et al, 2013;Rigato et al, 2015) have been published with the intention to use the levels of CEPCs as a prognosis for chronic kidney disease, cardiovascular disease, liver disease, retinopathy and vascular endothelial function. Hence, scarce data are available on the immunohistomorphology of microvascular ECs for CD34 and the expression of CEPCs for commonly used EC markers like CD31, CD34, CD45 and CD133 in the pancreas tissue in a diabetic rat, in comparison with that of the kidneys and liver.…”

Section: Introductionmentioning

confidence: 99%

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Immunohistomorphology of Pancreatic Islet Microvasculature and the Immunophenotypic Analysis of CEPC in Adult Diabetic Rats

et al. 2017

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TCHOKONTE-NANA, V.; LE ROUX, D. J.; KOTZE, P. C. & NGOUNOU, E.Immunohistomorphology of islet pancreatic microvasculature and the immunophenotypic analysis of CEPC in adult diabetic rats. Int. J. Morphol., 35(4):1560Morphol., 35(4): -1567Morphol., 35(4): , 2017. SUMMARY:Hyperglycaemia is one of the main causes for the endothelial cell (EC) damage in diabetic patients. Even though circulating endothelial progenitor cells (CEPC) could be used as a prognosis for microvascular complications, there is very little information on the islet microvasculature. We analysed by immunohistochemistry and by flow cytometric immunophenotyping, the expression of CD34 on EC and the expressions of CD31, CD34, CD45 and CD133 on CEPC in Streptozotocin (STZ)-induced diabetic rats. Peripheral blood and tissue specimens were obtained from rats of different treatment regimens: STZ treatment, control saline (NS) and sodium citrate (CB) treatments. Blood cells were exposed to flow cytometric immunophenotyping for CD133, CD31, CD34, CD45 and CD133. While tissues from the pancreas, liver and kidney were routinely processed and stained immunohistochemically for CD34. There was a tendency of an increased in CD45-/CD133+/CD31+/CD34+ cells (0.04 ± 0.11 %) in diabetic rats compared to the controls (CB: 0.03 ± 0.04 %; Saline: 0.01 ± 0.03 %). But there was no significant statistical difference between them. The expression pattern of CD34 on the EC in the organs' vascular beds including arterioles, venules, capillaries and sinusoids was extremely heterogeneous across and within treatment regimens. The ECs in the sinusoids of the liver presented similar CD34 expression patterns across different treatment regimens, while the expression of CD34 on the ECs of sinusoidal capillaries in the pancreas vary with the treatment regimen. We conclude that the degree of endothelial cell damage is not uniform across organs' vascular beds in the rat, contrary to mice and humans. Furthermore, the sinusoids in the pancreas and the kidney may have the same degree of endothelial damage when exposed to the same deleterious causes.

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Streptozotocin-Induced Diabetic Rat–Derived Bone Marrow Mesenchymal Stem Cells Have Impaired Abilities in Proliferation, Paracrine, Antiapoptosis, and Myogenic Differentiation

Cited by 80 publications

References 28 publications

Advanced Age Impairs Cardioprotective Function of Mesenchymal Stem Cell Transplantation from Patients to Myocardially Infarcted Rats

Advanced Age Impairs Cardioprotective Function of Mesenchymal Stem Cell Transplantation from Patients to Myocardially Infarcted Rats

Interrelationships of periodontitis and diabetes: A review of the current literature

Immunohistomorphology of Pancreatic Islet Microvasculature and the Immunophenotypic Analysis of CEPC in Adult Diabetic Rats

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