Exosomes derived from human placenta-derived mesenchymal stem cells improve neurologic function by promoting angiogenesis after spinal cord injury

Zhang, Ciliu; Zhang, ChengLiang; Xu, Yan; Liu, Chengjun; Cao, Yong; Li, Ping

doi:10.1016/j.neulet.2020.135399

Cited by 47 publications

(33 citation statements)

References 35 publications

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“…Exosomes are known to be secreted by multiple types of cells and may be associated with the progression of multiple diseases (45,46). Accumulating evidence has indicated that exosomes can create an immune suppressive environment by inducing inflammation (47,48).…”

Section: Discussionmentioning

confidence: 99%

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1

Wen

Tang

et al. 2021

Mol Med Rep

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Acute pancreatitis (AP) is one of the most frequent gastrointestinal diseases and has no specific treatment. It has been shown that dysfunction of pancreatic acinar cells can lead to AP progression. Emodin is a natural product, which can alleviate the symptoms of AP. However, the mechanism by which emodin regulates the function of pancreatic acinar cells remains unclear. Thus, the present study aimed to investigate the mechanism by which emodin modulates the function of pancreatic acinar cells. To mimic AP in vitro, pancreatic acinar cells were cotreated with caerulein and lipopolysaccharide (LPS). Exosomes were isolated using the ExoQuick precipitation kit. Western blot analysis, Nanosight Tracking analysis and transmission electron microscopy were performed to detect the efficiency of exosome separation. Gene expression was detected by reverse transcription-quantitative PCR. The levels of IL-1β and TNF-α were detected by ELISA. The data indicated that emodin significantly decreased the levels of IL-1β and TNF-α in the supernatant samples derived from AR42J cells cotreated with caerulein and LPS. In addition, emodin significantly promoted the proliferation of AR42J cells cotreated with caerulein and LPS, and inhibited apoptosis, while the effect of emodin was reversed by long non-coding (lnc)RNA taurine upregulated 1 (TUG1) overexpression. The expression level of TUG1 in AR42J cells or exosomes derived from AR42J cells was significantly increased following treatment of the cells with LPS and caerulein, while this effect was notably reversed by emodin treatment. In addition, exosomes derived from caerulein and LPS cotreated AR42J cells inhibited the differentiation and anti-inflammatory function of regulatory T cells, while treatment of the cells with emodin significantly decreased this effect. In conclusion, the data indicated that emodin inhibited the induction of inflammation in AR42J cells by regulating the expression of cellular and exosomal lncRNA. Therefore, emodin may be used as a potential agent for the treatment of AP.

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Section: Discussionmentioning

confidence: 99%

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1

Wen

Tang

et al. 2021

Mol Med Rep

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“…Zhang et al. [ 26 ] found that human placenta-derived mesenchymal stem cell derived exosomes support angiogenesis in SCI to augment neurologic function. These studies suggested that Shh upregulation or mesenchymal stem cell-derived exosome treatment is the hope for SCI repair.…”

Section: Discussionmentioning

confidence: 99%

Repair of spinal cord injury in rats via exosomes from bone mesenchymal stem cells requires sonic hedgehog

Jia

Yang

et al. 2021

Regenerative Therapy

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Objective The loss of neural ability leading to subsequent diminishing of motor function and the impairment below the location of the injury is a result of the SCI (Spinal Cord Injury). Among the many therapeutic agents for SCI, the exosomes considered as extracellular vesicles seem to be the most promising. Sonic Hedgehog (Shh) is an exosome-carrying protein. This Study's purpose was to identify whether Shh is required for exosomes from BMSCs (mesenchymal stem cells of the bone) and plays a protective effect on SCI. Methods Spinal cord injection with shRNA Shh-adeno associated virus (sh-Shh-AAV) were used to silence Shh. Exosomes were extracted from BMSCs. Rats that had suffered SCI were given intravenous injections of exosomes through the veins of the tail. Immunohistochemistry was used to identify the expression of Shh glycoprotein molecule as well as the expression of Gli-1 (glioma-associated oncogene homolog 1) in the rat spinal cord tissues. Western blot was performed to measure the levels of growth associated protein-43 (GAP-43). The BBB (Basso Beattie Bresnahan) score was used to assess the motor functions of the hind legs. In the same manner, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling or TUNEL and Nissl Staining was deployed to assess the level of regeneration of neurons and assess the level of histopathological damage in the tissues of the Spinal Cord. Results In the case of the rats with SCI, the levels of display of Gli-1 and Shh showed dramatic improvement after the BMSCs exosome injections. In comparison to rats with SCI, the subjects of BMSCs exosomes group showed an improvement in their SCI, including a higher BBB score and Nissl body count, increasing GAP-43 expression, along with a much-decreased number of cells that suffered apoptosis. While the exosome effect on Spinal Cord Injury was completely ineffective in rats that had Shh silencing. Conclusions Exosomes secreted from BMSCs showed great effectiveness in the SCI healing with a vital involvement of Shh in this repair.

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“…They have demonstrated that their administration promotes the tube formation and up‐regulates the motility of human umbilical vein endothelial cells (HUVEC). Furthermore, vessel number, vessel volume fraction, and vessel connectivity increased significantly after intrathecal injection of sEV in the mouse spinal cord injury model 47 …”

Section: Perspectives Of Using Msc‐derived Sev In Periodontologymentioning

confidence: 93%

Mesenchymal stem cell‐derived small extracellular vesicles as cell‐free therapy: Perspectives in periodontal regeneration

Novello

Pellen‐Mussi

Jeanne

2021

J of Periodontal Research

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Mesenchymal stem cells (MSC) are involved in the regeneration of the different missing or compromised periodontal tissues. MSC‐derived small extracellular vesicles (sEV) have recently been explored as a favorable substitution for stem cell therapy, as they are capable of producing therapeutic effects comparable to those of their parent cells, with advantages over cell therapy. The aim of this review is to evaluate the use of mesenchymal stem cells (MSC)‐derived sEV as cell‐free therapy in periodontal regeneration. A review of the scientific literature on sEV and their use in periodontal regeneration was performed. The main characteristics of sEV are described, and their mechanisms of action and potential biological effects in periodontal regeneration are studied. A summary of existing preclinical studies conducted in animals is performed. The results indicate that sEV derived from MSC are emerging as a promising new therapeutic tool in the field of periodontal regeneration and may become an ideal therapeutic option. In this review, we have summarized recent advances in this regard in order to better understand this newly emerging treatment. First results in vivo are promising and show a favorable potential for cell‐free therapy in periodontal regeneration.

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Exosomes derived from human placenta-derived mesenchymal stem cells improve neurologic function by promoting angiogenesis after spinal cord injury

Cited by 47 publications

References 35 publications

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1

Emodin inhibits the progression of acute pancreatitis via regulation of lncRNA TUG1 and exosomal lncRNA TUG1

Repair of spinal cord injury in rats via exosomes from bone mesenchymal stem cells requires sonic hedgehog

Mesenchymal stem cell‐derived small extracellular vesicles as cell‐free therapy: Perspectives in periodontal regeneration

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