A comparative study on the cellular stressors in mesenchymal stem cells (MSCs) and pancreatic β-cells under hyperglycemic milieu

Raghavan, Srividhya; Malayaperumal, Sarubala; Mohan, Viswanathan; Balasubramanyam, Muthuswamy

doi:10.1007/s11010-020-03922-4

Cited by 8 publications

(4 citation statements)

References 56 publications

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“…The role of BiP in cellular senescence is unclear since its levels were found to be increased 38,39 or decreased [40][41][42][43][44] depending on the cellular context. Moreover, two non-small cell lung cancer models displayed a different effect on HSPA5 expression in response to cisplatin induced senescence 45 .…”

Section: Discussionmentioning

confidence: 99%

The Endoplasmic Reticulum protein HSPA5/BiP is essential for decidual transformation of human endometrial stromal cells

Fernández,

Kong,

Alkhoury

et al. 2024

Preprint

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Decidualization denotes the process of inflammatory reprogramming of endometrial stromal cells (EnSC) into specialized decidual cells (DC). During this process, EnSC are subjected to endoplasmic reticulum (ER) stress as well as acute cellular senescence. Both processes contribute to the proinflammatory mid-luteal implantation window and their dysregulation has been implicated in reproductive failure. Here, we evaluated the link between ER stress, decidual differentiation and senescence. In-silico analysis identified HSPA5 gene, codifying the ER chaperone BiP, as a potentially critical regulator of cell fate divergence of decidualizing EnSC into anti-inflammatory DC and proinflammatory senescent decidual cells (snDC). Knockdown of HSPA5 in primary EnSC resulted both in decreased expression of DC marker genes and attenuated induction of senescence associated βgalactosidase activity, a marker of snDC. Stalling of the decidual reaction upon HSPA5 knockdown was apparent at 8 days of differentiation and was preceded by the upregulation of ER stress associated proteins IRE1α and PERK. Further, HSPA5 knockdown impaired colony-forming unit activity of primary EnSC, indicative of loss of cellular plasticity. Together, our results point to a key role for HSPA5/BiP in decidual transformation of EnSCs and highlight the importance of constraining ER stress levels during this process.

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Section: Discussionmentioning

confidence: 99%

The Endoplasmic Reticulum protein HSPA5/BiP is essential for decidual transformation of human endometrial stromal cells

Fernández,

Kong,

Alkhoury

et al. 2024

Preprint

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“…In high glucose culture conditions, the proliferation and migration of healthy BMMSCs are attenuated, while apoptosis is increased due to the involvement of the TGFα p38 MAPK signaling pathway [ 25 ] or activation of the GSK3b-mediated cyclin D1 [ 26 ]. Such decreased proliferation and migration is restored by treatment with metformin, a first line antihyperglycemic agent which also activates AMPK (AMP-activated protein kinase) [ 27 ]. Moreover, studies conducted on BMMSCs harvested from T1DM (Type 1 diabetes mellitus) rats reported limited clonogenicity and/or cell proliferation [ 28 , 29 , 30 , 31 ] and increased apoptosis [ 32 , 33 ].…”

Section: Discussionmentioning

confidence: 99%

Experimental Type 2 Diabetes Differently Impacts on the Select Functions of Bone Marrow-Derived Multipotent Stromal Cells

Ribot

Denoeud

Frescaline

et al. 2021

Cells

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Bone marrow-derived multipotent stromal cells (BMMSCs) represent an attractive therapeutic modality for cell therapy in type 2 diabetes mellitus (T2DM)-associated complications. T2DM changes the bone marrow environment; however, its effects on BMMSC properties remain unclear. The present study aimed at investigating select functions and differentiation of BMMSCs harvested from the T2DM microenvironment as potential candidates for regenerative medicine. BMMSCs were obtained from Zucker diabetic fatty (ZDF; an obese-T2DM model) rats and their lean littermates (ZL; controls), and cultured under normoglycemic conditions. The BMMSCs derived from ZDF animals were fewer in number, with limited clonogenicity (by 2-fold), adhesion (by 2.9-fold), proliferation (by 50%), migration capability (by 25%), and increased apoptosis rate (by 2.5-fold) compared to their ZL counterparts. Compared to the cultured ZL-BMMSCs, the ZDF-BMMSCs exhibited (i) enhanced adipogenic differentiation (increased number of lipid droplets by 2-fold; upregulation of the Pparg, AdipoQ, and Fabp genes), possibly due to having been primed to undergo such differentiation in vivo prior to cell isolation, and (ii) different angiogenesis-related gene expression in vitro and decreased proangiogenic potential after transplantation in nude mice. These results provided evidence that the T2DM environment impairs BMMSC expansion and select functions pertinent to their efficacy when used in autologous cell therapies.

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“…Recombinant human LF might be associated with the inhibition of ER stress in hepatocytes [ 9 ]. Raghavan et al [ 130 ] reported that high glucose (HG) significantly increased the mRNA level of ER stress markers such as GRP78, CHOP, IRE1, and PERK, whereas only XBP1 rises transiently in pancreatic beta-cells. Interestingly, these were significantly reduced by treatment of LF.…”

Section: Pharmacological Potentials Of Lactoferrin Against Various Pathophysiological Conditions In Kidney Diseasesmentioning

confidence: 99%

“…In mesenchymal stem cells, HG also significantly increased the mRNA level of GRP78, IRE1, and PERK, whereas only IRE1 and XBP1 rise transiently. LF treatment significantly decreased those ER stress markers except XBP1 [ 130 ]. Since, no study regarding LF against ER stress in kidney cells has been found, further study is required to check whether LF can protect the kidney against ER stress-induced cellular damage.…”

Section: Pharmacological Potentials Of Lactoferrin Against Various Pathophysiological Conditions In Kidney Diseasesmentioning

confidence: 99%

Kidney protective potential of lactoferrin: pharmacological insights and therapeutic advances

Zahan¹,

Ahmed²,

Moni³

et al. 2022

Korean J Physiol Pharmacol

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Kidney disease is becoming a global public health issue. Acute kidney injury (AKI) and chronic kidney disease (CKD) have serious adverse health outcomes. However, there is no effective therapy to treat these diseases. Lactoferrin (LF), a multi-functional glycoprotein, is protective against various pathophysiological conditions in various disease models. LF shows protective effects against AKI and CKD. LF reduces markers related to inflammation, oxidative stress, apoptosis, and kidney fibrosis, and induces autophagy and mitochondrial biogenesis in the kidney. Although there are no clinical trials of LF to treat kidney disease, several clinical trials and studies on LF-based drug development are ongoing. In this review, we discussed the possible kidney protective mechanisms of LF, as well as the pharmacological and therapeutic advances. The evidence suggests that LF may become a potent pharmacological agent to treat kidney diseases.

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A comparative study on the cellular stressors in mesenchymal stem cells (MSCs) and pancreatic β-cells under hyperglycemic milieu

Cited by 8 publications

References 56 publications

The Endoplasmic Reticulum protein HSPA5/BiP is essential for decidual transformation of human endometrial stromal cells

The Endoplasmic Reticulum protein HSPA5/BiP is essential for decidual transformation of human endometrial stromal cells

Experimental Type 2 Diabetes Differently Impacts on the Select Functions of Bone Marrow-Derived Multipotent Stromal Cells

Kidney protective potential of lactoferrin: pharmacological insights and therapeutic advances

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