Down-regulation of miR-34a alleviates mesangial proliferation in vitro and glomerular hypertrophy in early diabetic nephropathy mice by targeting GAS1

Zhang, Le; He, Siyi; Guo, Shaodong; Xie, Wei; Rong, Xianglu; Yu, Hua; Yang, Fan; Qiu, Jing; Zhang, Di; Zhou, Shiwen; Zhang, Kebin

doi:10.1016/j.jdiacomp.2014.01.002

Cited by 66 publications

(46 citation statements)

References 32 publications

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“…miRNAs have been implicated in the epigenetic regulation of key metabolic, inflammatory, and antiangiogenic pathways in T2DM. Zhang et al (29) demonstrated that miR-34a could regulate mesangial proliferation and glomerular hypertrophy by directly inhibiting GAS1 in early diabetic nephropathy (DN). A further study has ascertained that miR-34a was able to inhibit osteosarcoma growth through the downregulation of Eag1 expression (17).…”

Section: Discussionmentioning

confidence: 99%

miR‑34a and miR‑125b are upregulated in peripheral blood mononuclear cells from patients with type 2 diabetes mellitus

Yan-xin

Pan

et al. 2017

Exp Ther Med

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Abstract. Type 2 diabetes mellitus (T2DM) is a leading cause of blindness, non-traumatic amputation and end-stage renal disease, as well as a major cardiovascular risk factor. To determine whether miR-125b and miR-34a serve an important role in the development of T2DM, the current study investigated the expression profile of two microRNAs (miR-34a and miR-125b) and their relative genes in peripheral blood mononuclear cells from 73 patients with T2DM and 52 healthy donors by reverse transcription-quantitative polymerase chain reaction In addition, the association between miR-34a, miR-125b and their relevant genes expression profile were analyzed with respect to the pathogenesis of T2DM. The present study demonstrated that the expression levels of miR-125b and miR-34a were elevated in peripheral blood mononuclear cell samples from patients with T2DM. Furthermore, miR-34a and miR-125b were positively correlated with low-density lipoprotein/high-density lipoprotein (HDL) and Foxp3 and negatively related to triglyceride/HDL. However, no correlation among miR-34a, miR-125b and the value of homeostasis model assessment of insulin resistance, homeostasis model assessment of β-cell function and the genes of B lymphocyte-induced maturation protein-1, interferon regulatory factor-4, P53 and retinoid-related orphan receptor γt were observed. These results indicate that the alteration of miR-34a and miR-125b exists in patients with T2DM, which may be involved in the pathogenesis of T2DM, and could be a potential novel biomarker of T2DM. IntroductionType 2 diabetes mellitus (T2DM), formerly termed non-insulin-dependent diabetes mellitus or adult-onset diabetes, is a multifactor disease that involves complex interactions between genes (1-3), abnormalities of the immune system (4-6), environmental factors (7-10) and health-impacting behavior (11,12), and represents a serious public health problem in numerous developed countries (13). Current investigations have revealed a definite global increase in the incidence and prevalence of diabetes. In 2013, 382 million people worldwide were estimated to be diabetic by the International Diabetes Federation, which is expected to rise to 592 million cases in the year 2035 (14). As a result of the increasing rate of diabetes and its widespread societal and economic consequences, prevention of diabetes among people at high risk is an important public health issue in clinic practice. However, the extent to which multiple defects in the regulation of lipids, insulin secretion and action, and the immune system contribute to the pathogenesis of T2DM has yet to be elucidated.MicroRNAs (miRNAs) are a class of small, single-stranded non-coding RNAs (~22 nucleotides) that are transcribed from the DNA of a gene, and modulate the expression of a network of mRNAs through binding to the 3'-untranslated region (3'-UTR), 5'-UTR or to the open reading frame of target mRNAs (15). Notably, each miRNA is able to target multiple mRNAs. Growing evidence indicates that miRNAs are involved in T2DM (16). However,...

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Section: Discussionmentioning

confidence: 99%

miR‑34a and miR‑125b are upregulated in peripheral blood mononuclear cells from patients with type 2 diabetes mellitus

Yan-xin

Pan

et al. 2017

Exp Ther Med

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“…Furthermore, high glucose in vitro and diabetes in animals result in increased expression of miR‐34a, an event that could be related to the development of diabetic nephropathy (Zhang et al . ).…”

Section: Introductionmentioning

confidence: 97%

Diabetes and ageing‐induced vascular inflammation

Assar

Angulo

Rodríguez‐Mañas

2015

The Journal of Physiology

100

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Diabetes and the ageing process independently increase the risk for cardiovascular disease (CVD). Since incidence of diabetes increases as people get older, the diabetic older adults represent the largest population of diabetic subjects. This group of patients would potentially be threatened by the development of CVD related to both ageing and diabetes. The relationship between CVD, ageing and diabetes is explained by the negative impact of these conditions on vascular function. Functional and clinical evidence supports the role of vascular inflammation induced by the ageing process and by diabetes in vascular impairment and CVD. Inflammatory mechanisms in both aged and diabetic vasculature include pro‐inflammatory cytokines, vascular hyperactivation of nuclear factor‐кB, increased expression of cyclooxygenase and inducible nitric oxide synthase, imbalanced expression of pro/anti‐inflammatory microRNAs, and dysfunctional stress‐response systems (sirtuins, Nrf2). In contrast, there are scarce data regarding the interaction of these mechanisms when ageing and diabetes co‐exist and its impact on vascular function. Older diabetic animals and humans display higher vascular impairment and CVD risk than those either aged or diabetic, suggesting that chronic low‐grade inflammation in ageing creates a vascular environment favouring the mechanisms of vascular damage driven by diabetes. Further research is needed to determine the specific inflammatory mechanisms responsible for exacerbated vascular impairment in older diabetic subjects in order to design effective therapeutic interventions to minimize the impact of vascular inflammation. This would help to prevent or delay CVD and the specific clinical manifestations (cognitive decline, frailty and disability) promoted by diabetes‐induced vascular impairment in the elderly.

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“…[24][25][26][27] As a hallmark event, MC hypertrophy caused concerns at a very early stage of DN. Limiting its early growth might have impact on the later progression of DN.…”

Section: Discussionmentioning

confidence: 99%

MiR-196a Regulates High Glucose-Induced Mesangial Cell Hypertrophy by Targeting p27kip1

et al. 2015

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Down-regulation of miR-34a alleviates mesangial proliferation in vitro and glomerular hypertrophy in early diabetic nephropathy mice by targeting GAS1

Cited by 66 publications

References 32 publications

miR‑34a and miR‑125b are upregulated in peripheral blood mononuclear cells from patients with type 2 diabetes mellitus

miR‑34a and miR‑125b are upregulated in peripheral blood mononuclear cells from patients with type 2 diabetes mellitus

Diabetes and ageing‐induced vascular inflammation

MiR-196a Regulates High Glucose-Induced Mesangial Cell Hypertrophy by Targeting p27kip1

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