Recent Advances in Stem Cell Research in Subarachnoid Hemorrhage

Song, Zhijun; Zhang, Junyi

doi:10.1089/scd.2019.0219

Cited by 11 publications

(7 citation statements)

References 79 publications

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“…In pre-clinical studies, novel treatment possibilities affecting TLR4 have proved to be extremely effective for preventing SAH and its associated effects. Of note, current research indicates that exploiting stem cell technologies presents a scientific rationale, and with the recent penetration of clinical applications of neural stem cell transplantation, this translates into a feasible option to treat SAH and post-treatment complications [70]. As miss-regulation of microglial MyD88 signaling was shown to misbalance neural stem cell maintenance in the hippocampus [71], any neuro-repair or general cell-based endeavors to treatment of SAH should carefully monitor, and ideally, control MyD88 activity in the cell therapeutics and/or host tissue, respectively.…”

Section: Discussionmentioning

confidence: 99%

Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation: A Systematic Review

Ahmed

Khan

Kahlert

et al. 2021

IJMS

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Myeloid differentiation 88 (MyD88) is a well-established inflammatory adaptor protein. It is one of the essential downstream proteins of the toll-like receptor 4 (TLR4) signaling pathway. TLRs are pattern recognition receptors that are usually activated by the damage-associated molecular pattern molecules (DAMPs). Sterile inflammation is triggered by the endogenous DAMPs released in response to global cerebral ischemia and from extravasated blood after subarachnoid hemorrhage (SAH). In this review, we highlight the importance of the neuroinflammatory role of the MyD88 in the SAH. We also explore a few possible pharmacological agents that can be used to decrease SAH-associated neuroinflammation by modulating the MyD88 dependent functions. Pharmacological agents such as flavonoids, melatonin, fluoxetine, pentoxifylline and progesterone have been investigated experimentally to reduce the SAH-associated inflammation. Inhibition of the MyD88 not only reduces the expression of pro-inflammatory cytokines, but also potentially inhibits other processes that can augment the SAH associated inflammation. Further investigations are required to translate these findings in the clinical setting.

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Section: Discussionmentioning

confidence: 99%

Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation: A Systematic Review

Ahmed

Khan

Kahlert

et al. 2021

IJMS

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“…IA is a disease of intracranial arterial dilatation. When the arterial wall is impacted by haemodynamic shear force and a series of pathophysiological changes, the arterial blood vessels will swell and protrude until an aneurysm is formed 3 , 5 – 7 . Some IAs are relatively stable due to special anatomical locations, whilst other IAs are due to the death or loss of parietal cells or degeneration of the extracellular matrix, which eventually leads to the rupture of the vascular wall 14 , 15 .…”

Section: Discussionmentioning

confidence: 99%

“…Intracranial aneurysm (IA) is a common cerebrovascular disease, and its incidence has been increasing year by year 1 , 2 . Spontaneous subarachnoid haemorrhage (SAH) caused by IA and cerebral haemorrhage induced by a rupture have high mortality rates 3 – 6 . Although nerve intervention and microscopy techniques have been developed, the disability and fatality rate of IA remain as high as 30–40% 7 .…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-513b-5p targets COL1A1 and COL1A2 associated with the formation and rupture of intracranial aneurysm

Zhang

Chen

Wang

et al. 2021

Sci Rep

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Collagen-type I alpha 1 chain (COL1A1) and COL1A2 are abnormally expressed in intracranial aneurysm (IA), but their mechanism of action remains unclear. This study was performed to investigate the mechanism of COL1A1 and COL1A2 affecting the occurrence and rupture of IA. Quantitative real-time polymerase chain reaction was used to measure the expression of hsa-miR-513b-5p, COL1A1, COL1A2, TNF-α, IL-6, MMP2, MMP3, MMP9 and TIMP4 in patients with ruptured IA (RA) (n = 100), patients with un-ruptured IA (UA) (n = 100), and controls (n = 100). Then, human vascular smooth muscle cells (HASMCs) were cultured, and dual luciferase reporter assay was performed to analyse the targeting relationship between miR-513b-5p and COL1A1 or COL1A2. The effects of the miR-513b-5p mimic and inhibitor on the proliferation, apoptosis, and death of HASMC and the RIP1-RIP3-MLKL and matrix metalloproteinase pathways were also explored. The effect of silencing and over-expression of COL1A1 and COL1A2 on the role of miR-513b-5p were also evaluated. Finally, the effects of TNF-α on miR-513b-5p targeting COL1A1 and COL1A2 were tested. Compared with those in the control group, the serum mRNA levels of miR-513b-5p, IL-6 and TIMP4 were significantly decreased in the RA and UA groups, but COL1A1, COL1A2, TNF-α, IL-1β, MMP2, MMP3 and MMP9 were significantly increased (p < 0.05). Compared with those in the UA group, the expression of COL1A1, COL1A2, TNF-α, IL-1β and MMP9 was significantly up-regulated in the RA group (p < 0.05). Results from the luciferase reporter assay showed that COL1A1 and COL1A were the direct targets of miR-513b-5p. Further studies demonstrated that miR-513b-5p targeted COL1A1/2 to regulate the RIP1-RIP3-MLKL and MMP pathways, thereby enhancing cell death and apoptosis. Over-expression of COL1A1 or COL1A2, rather than silencing COL1A1/2, could improve the inhibitory effect of miR-513b-5p on cell activity by regulating the RIP1-RIP3-MLKL and MMP pathways. Furthermore, over-expression of miR-513b-5p and/or silencing COL1A1/2 inhibited the TNF-α-induced cell proliferation and enhanced the TNF-α-induced cell death and apoptosis. The mechanism may be related to the inhibition of collagen I and TIMP4 expression and promotion of the expression of RIP1, p-RIP1, p-RIP3, p-MLKL, MMP2 and MMP9. MiR-513b-5p targeted the inhibition of COL1A1/2 expression and affected HASMC viability and extracellular mechanism remodelling by regulating the RIP1-RIP3-MLKL and MMP pathways. This process might be involved in the formation and rupture of IA.

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“…In recent years, researchers raised the concern about the beneficial effect of stem cell therapy in SAH [ 11 ]. The easy accessibility and potent paracrine activities have made mesenchymal stem cells (MSCs) an increasingly popular candidate for the treatment of SAH in comparison with other stem cell types.…”

Section: Introductionmentioning

confidence: 99%

Mesenchymal stem cells-derived therapies for subarachnoid hemorrhage in preclinical rodent models: a meta-analysis

Jianyang

Huang

et al. 2022

Stem Cell Res Ther

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Background Mesenchymal stem cells (MSCs) and MSCs-derived extracellular vesicles (EVs) have emerged as potential novel therapies for subarachnoid hemorrhage (SAH). However, their effects remain incompletely understood. We aim to comprehensively evaluate the effect of MSCs-derived therapies in rodent models of SAH. Methods We searched PubMed, EMBASE, and Web of Science up to September 2021 to identify studies that reported the effects of MSCs or MSCs-derived EVs in a rodent SAH model. Neurobehavioral score was extracted as the functional outcome, and brain water content was measured as the histopathological outcome. A random-effects model was used to calculate the standardized mean difference (SMD) and confidence interval (CI). Results Nine studies published from 2018 to 2021 met the inclusion criteria. Studies quality scores ranged from 5 to 10, with a mean value of 7.22. Our results revealed an overall positive effect of MSCs and MSCs-derived EVs on the neurobehavioral score with a SMD of − 2.21 (95% CI − 3.14, − 1.08; p < 0.0001). Meanwhile, we also found that MSCs and MSCs-derived EVs reduced brain water content by a SMD of − 2.09 (95% CI − 2.99, − 1.19; p < 0.00001). Significant heterogeneity among studies was observed, further stratified and sensitivity analyses did not identify the source of heterogeneity. Conclusions Our results suggested that MSCs-derived therapies prominently improved functional recovery and reduced brain edema in the rodent models of SAH. Notably, the limitations of small sample size should be considered when interpreting the results, and large animal studies and human trials are needed for further investigation.

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Recent Advances in Stem Cell Research in Subarachnoid Hemorrhage

Cited by 11 publications

References 79 publications

Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation: A Systematic Review

Role of Adaptor Protein Myeloid Differentiation 88 (MyD88) in Post-Subarachnoid Hemorrhage Inflammation: A Systematic Review

MicroRNA-513b-5p targets COL1A1 and COL1A2 associated with the formation and rupture of intracranial aneurysm

Mesenchymal stem cells-derived therapies for subarachnoid hemorrhage in preclinical rodent models: a meta-analysis

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