The microRNA-dependent cell fate of multipotent stromal cells differentiating to endothelial cells

Cha, Min‐Ji; Choi, Eun Kyoung; Lee, Seahyoung; Song, Bomi; Yoon, Cheesoon; Hwang, Ki‐Chul

doi:10.1016/j.yexcr.2016.02.005

Cited by 4 publications

(3 citation statements)

References 51 publications

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“…Moreover, cardiogenic miRNAs, like miR-499 and miR-133 have been demonstrated to stimulate the cardiac differentiation of MSCs, including up-regulation of NKX2.5 and GATA-4 51 , 52 . Future studies are needed to identify the miRNA candidates involved in the lineage specification of MSCs, which can be further used for their preconditioning and thereby promoting the cardiogenic potential 53 .…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of stem cell based cardiac repair-gap junctional signaling promotes the cardiac lineage specification of mesenchymal stem cells

Lemcke

Gaebel

Skorska

et al. 2017

Sci Rep

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Different subtypes of bone marrow-derived stem cells are characterized by varying functionality and activity after transplantation into the infarcted heart. Improvement of stem cell therapeutics requires deep knowledge about the mechanisms that mediate the benefits of stem cell treatment. Here, we demonstrated that co-transplantation of mesenchymal stem cells (MSCs) and hematopoietic stem cells (HSCs) led to enhanced synergistic effects on cardiac remodeling. While HSCs were associated with blood vessel formation, MSCs were found to possess transdifferentiation capacity. This cardiomyogenic plasticity of MSCs was strongly promoted by a gap junction-dependent crosstalk between myocytes and stem cells. The inhibition of cell-cell coupling significantly reduced the expression of the cardiac specific transcription factors NKX2.5 and GATA4. Interestingly, we observed that small non-coding RNAs are exchanged between MSCs and cardiomyocytes in a GJ-dependent manner that might contribute to the transdifferentiation process of MSCs within a cardiac environment. Our results suggest that the predominant mechanism of HSCs contribution to cardiac regeneration is based on their ability to regulate angiogenesis. In contrast, transplanted MSCs have the capability for intercellular communication with surrounding cardiomyocytes, which triggers the intrinsic program of cardiogenic lineage specification of MSCs by providing cardiomyocyte-derived cues.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of stem cell based cardiac repair-gap junctional signaling promotes the cardiac lineage specification of mesenchymal stem cells

Lemcke

Gaebel

Skorska

et al. 2017

Sci Rep

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“…Moreover, it is possible that the activation of FAK signaling increased the FGFR expression as previously reported, [ 46 ] and the FGFR is involved in the activation of its downstream signals of Akt or mTOR, which induce the expression of the endothelial markers, such as Flk‐1, CD31, and Ac‐LDL. [ 47–49 ] However, the detailed mechanisms for the promotion of the proliferation and endothelial differentiation in response to the dual‐scale crossed sinusoidal wavy patterns should be elucidated through further study.…”

Section: Resultsmentioning

confidence: 99%

Micro/Nano Dual‐Scale Crossed Sinusoidal Wavy Patterns for Synergistic Promotion of Proliferation and Endothelial Differentiation of Human Adipose‐Derived Stem Cells

Kim

Lee

Park

et al. 2020

Adv Materials Inter

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Although human adipose‐derived stem cells (hASCs) have great potential as a cell source for stem cell therapy due to their capacity of self‐renewal, long‐term growth, and multipotency with high obtainability through lipoaspiration, little is known about the effects of micro/nano dual‐scale topography on the proliferation and differentiation of the hASCs. In this study, the effects of micro/nano dual‐scale crossed sinusoidal wavy patterns (SIMNs) on the hASC behaviors including cellular alignment, proliferation, and endothelial differentiation are investigated. Various types of microscale, nanoscale, and SIMNs are fabricated on a single polystyrene surface in a step‐gradient manner based on the combined fabrication processes of deep X‐ray lithography, polydimethylsiloxane surface wrinkling, and thermal nanoimprinting process. The cellular alignment, proliferation, and endothelial differentiation of the hASCs are promoted on the SIMNs compared to the microscale or nanoscale sinusoidal wavy patterns. A micro/nano dual‐scale pattern of SIMN160_500, which has a micro‐scale sinusoidal wavy pattern with a wavelength of 160 µm crossed with a nanoscale sinusoidal wavy pattern with a wavelength of 500 nm, is found to be a most effective pattern for synergistically promoting both proliferation and endothelial differentiation of the hASCs with 1.2‐fold and 2‐fold increases, respectively.

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“…Beyond pharmacological treatment, the effect on autophagy activation by miR-26a silencing was a consequence of the deficiency in the endothelial recovery, associated with the absence of miR-26a dependent differentiation of mesenchymal stem cells in functional endothelial cells. This deficiency, reducing tumor blood flow, favored the Warburg effect in the TME [150]. Indeed, miR-26a re-expression sensitized melanoma cell lines to dabrafenib, targeting the high mobility group box 1 (HMGB1)-dependent autophagy, and finally, engaging the apoptosis program [131].…”

Section: Melanomamentioning

confidence: 99%

The Sex-Related Interplay between TME and Cancer: On the Critical Role of Estrogen, MicroRNAs and Autophagy

Matarrese

Mattia

Pagano

et al. 2021

Cancers

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The interplay between cancer cells and the tumor microenvironment (TME) has a fundamental role in tumor progression and response to therapy. The plethora of components constituting the TME, such as stroma, fibroblasts, endothelial and immune cells, as well as macromolecules, e.g., hormones and cytokines, and epigenetic factors, such as microRNAs, can modulate the survival or death of cancer cells. Actually, the TME can stimulate the genetically regulated programs that the cell puts in place under stress: apoptosis or, of interest here, autophagy. However, the implication of autophagy in tumor growth appears still undefined. Autophagy mainly represents a cyto-protective mechanism that allows cell survival but, in certain circumstances, also leads to the blocking of cell cycle progression, possibly leading to cell death. Since significant sex/gender differences in the incidence, progression and response to cancer therapy have been widely described in the literature, in this review, we analyzed the roles played by key components of the TME, e.g., estrogen and microRNAs, on autophagy regulation from a sex/gender-based perspective. We focused our attention on four paradigmatic and different forms of cancers—colon cancer, melanoma, lymphoma, and lung cancer—concluding that sex-specific differences may exert a significant impact on TME/cancer interaction and, thus, tumor growth.

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The microRNA-dependent cell fate of multipotent stromal cells differentiating to endothelial cells

Cited by 4 publications

References 51 publications

Mechanisms of stem cell based cardiac repair-gap junctional signaling promotes the cardiac lineage specification of mesenchymal stem cells

Mechanisms of stem cell based cardiac repair-gap junctional signaling promotes the cardiac lineage specification of mesenchymal stem cells

Micro/Nano Dual‐Scale Crossed Sinusoidal Wavy Patterns for Synergistic Promotion of Proliferation and Endothelial Differentiation of Human Adipose‐Derived Stem Cells

The Sex-Related Interplay between TME and Cancer: On the Critical Role of Estrogen, MicroRNAs and Autophagy

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