Comparative analysis of gene expression profiles in children with type 1 diabetes mellitus

Qian, Liwei; Shi, Honglei; Ding, Mei-Li

doi:10.3892/mmr.2019.10099

Cited by 9 publications

(10 citation statements)

References 61 publications

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“…Cytokine-induced HNRNPD expression has been linked with increased rates of beta cell apoptosis in patients with diabetes [19], while reduced HNRNPD expression is linked to survival of pancreatic beta cells [25]. Reduced expression of HNRNPD has been reported in the blood of children with T1D and is thought to be associated with disease progression [26]. Finally, HNRNPD has also linked with senescence [27], which is an emerging new driver of both T1D and T2D [28,29].…”

Section: Discussionmentioning

confidence: 99%

Changes to the identity of EndoC-βH1 beta cells may be mediated by stress-induced depletion of HNRNPD

et al. 2021

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Background Beta cell identity changes occur in the islets of donors with diabetes, but the molecular basis of this remains unclear. Protecting residual functional beta cells from cell identity changes may be beneficial for patients with diabetes. Results A somatostatin-positive cell population was induced in stressed clonal human EndoC-βH1 beta cells and was isolated using FACS. A transcriptomic characterisation of somatostatin-positive cells was then carried out. Gain of somatostatin-positivity was associated with marked dysregulation of the non-coding genome. Very few coding genes were differentially expressed. Potential candidate effector genes were assessed by targeted gene knockdown. Targeted knockdown of the HNRNPD gene induced the emergence of a somatostatin-positive cell population in clonal EndoC-βH1 beta cells comparable with that we have previously reported in stressed cells. Conclusions We report here a role for the HNRNPD gene in determination of beta cell identity in response to cellular stress. These findings widen our understanding of the role of RNA binding proteins and RNA biology in determining cell identity and may be important for protecting remaining beta cell reserve in diabetes.

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Section: Discussionmentioning

confidence: 99%

Changes to the identity of EndoC-βH1 beta cells may be mediated by stress-induced depletion of HNRNPD

et al. 2021

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“…DNA methylation patterns can be altered by a number of environmental factors including hyperglycaemia, which may change the expression of coding genes as well as microRNA (miRNA) profile in target cell (Gan et al, 2020; Kan et al, 2018; Yao et al, 2019). Therefore, uncontrolled DM has the potential to alter gene expression profile and thus may impact signalling and molecular pathways in a variety of tissues (Chen et al, 2019; Gastol et al, 2020; Lu et al, 2020; Mishra et al, 2017; Qian et al, 2019). Such non‐physiological epigenetic modifications in DM may play a key role in the development of neurological complications by altering the gene expression and miRNA pattern in nervous tissue (Gan et al, 2020; Kan et al, 2018; Qian et al, 2019; Yao et al, 2019; Figure 4).…”

Section: The Rage Diaph1 and Another Rage Ligands In Neurological Complications Of Dmmentioning

confidence: 99%

“…Therefore, uncontrolled DM has the potential to alter gene expression profile and thus may impact signalling and molecular pathways in a variety of tissues (Chen et al, 2019; Gastol et al, 2020; Lu et al, 2020; Mishra et al, 2017; Qian et al, 2019). Such non‐physiological epigenetic modifications in DM may play a key role in the development of neurological complications by altering the gene expression and miRNA pattern in nervous tissue (Gan et al, 2020; Kan et al, 2018; Qian et al, 2019; Yao et al, 2019; Figure 4).…”

Section: The Rage Diaph1 and Another Rage Ligands In Neurological Complications Of Dmmentioning

confidence: 99%

“…Further, studies have revealed association of DIAPH1 gene polymorphisms with ischaemic stroke, macrothrombocytopenia and deafness (Egaña‐Gorroño et al, 2020; Ercan‐Sencicek et al, 2015; Ren et al, 2019). Moreover, comparative analysis of gene expression profiles in children with Type 1 diabetes have revealed that Rho GTPase‐activating protein 25, encoded by the ARHGAP25 gene, is upregulated in patients with diabetes (Qian et al, 2019). The ARHGAP25 belongs to a family of Rho GTPase just like DIAPH1 (Katoh & Katoh, 2004; Mao, 2011).…”

Section: The Rage Diaph1 and Another Rage Ligands In Neurological Complications Of Dmmentioning

confidence: 99%

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The cross‐talk between RAGE and DIAPH1 in neurological complications of diabetes: A review

Zglejc-Waszak

Mukherjee

Juranek

2021

Eur J of Neuroscience

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Neuropathy, or dysfunction of peripheral nerve, is one of the most common neurological manifestation in patients with diabetes mellitus (DM). DM is typically associated with a hyperglycaemic milieu, which promotes non‐enzymatic glycation of proteins. Proteins with advanced glycation are known to engage a cell‐surface receptor called the receptor for advanced glycation end products (RAGE). Thus, it is reasonable to assume that RAGE and its associated molecule‐mediated cellular signalling may contribute to DM‐induced symmetrical axonal (length‐dependent) neuropathy. Of particular interest is diaphanous related formin 1 (DIAPH1), a cytoskeletal organizing molecule, which interacts with the cytosolic domain of RAGE and whose dysfunction may precipitate axonopathy/neuropathy. Indeed, it has been demonstrated that both RAGE and DIAPH1 are expressed in the motor and sensory fibres of nerve harvested from DM animal models. Although the detailed molecular role of RAGE and DIAPH1 in diabetic neurological complications remains unclear, here we will discuss available evidence of their involvement in peripheral diabetic neuropathy. Specifically, we will discuss how a hyperglycaemic environment is not only likely to elevate advanced glycation end products (ligands of RAGE) and induce a pro‐inflammatory environment but also alter signalling via RAGE and DIAPH1. Further, hyperglycaemia may regulate epigenetic mechanisms that interacts with RAGE signalling. We suggest the cumulative effect of hyperglycaemia on RAGE–DIAPH1‐mediated signalling may be disruptive to axonal cytoskeletal organization and transport and is therefore likely to play a key role in pathogenesis of diabetic symmetrical axonal neuropathy.

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“…Contudo, as principais complicações tardias comuns em portadores de diabetes são a micro e macroangiopatia, aterosclerose, nefropatia, retinopatia (SHULMAN; LUO; SHAH, 2018) e neuropatia (ASLAN et al, 2019 O DM1 surge em decorrência da destruição autoimune das células β do pâncreas, responsáveis pela produção de insulina. Neste caso, as ilhotas são infiltradas por macrófagos, linfócitos, células dendríticas e linfócitos Natural Killer (NK); além da alta expressão de vários genes do sistema imunológico (QIAN;SHI;DING, 2019).…”

Section: Diabetes Mellitusunclassified

Implications of Vitamin D Insufficiency/Deficiency in Autoimmune Diseases: A Review

Alves¹,

Cesilio²,

Alves³

et al. 2021

Rev. UNINGÁ

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A vitamina D é um hormônio esteroide lipossolúvel com amplitude de efeitos biológicos que extrapolam a regulação do metabolismo do cálcio e da saúde óssea, que alcança preponderante papel na manutenção da homeostase sistêmica, relacionado ao crescimento, diferenciação e apoptose celular, regulação dos sistemas imunológico, cardiovascular e muscular e ao metabolismo da insulina; além de participar da modulação direta ou indireta de cerca de 3% do genoma humano. Frente o exposto, e considerando as graves complicações advindas da deficiência de vitamina D para a saúde e qualidade de vida, propôs-se neste trabalho um estudo descritivo, o qual relaciona a insuficiência/deficiência desta vitamina a algumas doenças autoimunes como o lúpus eritematoso sistêmico, o diabetes mellitus, a esclerose múltipla, a artrite reumatoide e a doença inflamatória intestinal (Doença de Crohn). Este estudo foi desenvolvido a partir de 58 artigos, dentre os quais incluem os de revisão, artigos originais de pesquisas clínicas e experimentais, publicados entre 2008 a 2020, obtidos a partir da pesquisa no banco de dados Pubmed®, Google Acadêmico e Scientific Electronic Library Online (SCIELO). Com base nos estudos relacionados às doenças autoimunes, pode-se concluir que a vitamina D exibe função imunomoduladora crucial, garantindo eficiente sistema de proteção. Estudos que versam sobre a suplementação de vitamina D, tanto para a prevenção quanto para o tratamento das doenças autoimunes existentes são necessários e de grande valia para o entendimento dessas implicações.

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Comparative analysis of gene expression profiles in children with type 1 diabetes mellitus

Cited by 9 publications

References 61 publications

Changes to the identity of EndoC-βH1 beta cells may be mediated by stress-induced depletion of HNRNPD

Changes to the identity of EndoC-βH1 beta cells may be mediated by stress-induced depletion of HNRNPD

The cross‐talk between RAGE and DIAPH1 in neurological complications of diabetes: A review

Implications of Vitamin D Insufficiency/Deficiency in Autoimmune Diseases: A Review

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