The effect of administration of double stranded MicroRNA-210 on acceleration of Achilles tendon healing in a rat model

Usman, Munyati; Nakasa, Tomoyuki; Shoji, Takeshi; Kato, Tomohiro; Kawanishi, Yoshitaka; Hamanishi, Michio; Kamei, Naosuke; Ochi, Mitsuo

doi:10.1007/s00776-015-0709-5

Cited by 27 publications

(31 citation statements)

References 28 publications

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“…MicroRNA acts through posttranscriptional regulation of target genes, leading to the degradation of target gene mRNAs or translational inhibition. The results from this study and previous studies showed increased VEGF and STAT3 expression when miR‐210 was overexpressed . Consequently, we hypothesized that VEGF and STAT3 may not be direct targets of miR‐210.…”

Section: Resultssupporting

confidence: 48%

“…The results from this study and previous studies showed increased VEGF and STAT3 expression when miR-210 was overexpressed. 30,31,33 Consequently, we hypothesized that VEGF and STAT3 may not be direct targets of miR-210. Through bioinformatics analysis, we found that miR-210 can bind to the 3 0 -UTR of SOCS1 mRNA, and SOCS1 may be the downstream target gene of miR-210.…”

Section: Stat3-vegf Activation Is Modulated By Mir-210 Through Socs1 mentioning

confidence: 99%

“…VEGF and VEGF receptor (VEGFR) expression is upregulated in the ischemic penumbra, which is beneficial for neurovascular remodeling and neurological function recovery after a hypoxic/ischemic cerebral injury . Several studies indicated that miR‐210 upregulates VEGF expression . Therefore, we hypothesized that EPC homing may be involved in cerebral neovascularization following cerebral ischemia and that miR‐210 in EPCs upregulates VEGF under hypoxic conditions, promoting NPC accumulation and survival around ischemic foci and neurological function recovery.…”

Section: Introductionmentioning

confidence: 99%

“…17,[23][24][25][26][27][28][29] Several studies indicated that miR-210 upregulates VEGF expression. [30][31][32][33] Therefore, we hypothesized that EPC homing may be involved in cerebral neovascularization following cerebral ischemia and that miR-210 in EPCs upregulates VEGF under hypoxic conditions, promoting NPC accumulation and survival around ischemic foci and neurological function recovery.…”

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confidence: 99%

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MicroRNA‐210 Promotes Accumulation of Neural Precursor Cells Around Ischemic Foci After Cerebral Ischemia by Regulating the SOCS1–STAT3–VEGF‐C Pathway

Meng

Kang

Duan

et al. 2018

JAHA

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BackgroundNeural precursor cell (NPC) migration toward lesions is key for neurological functional recovery. The neovasculature plays an important role in guiding NPC migration. MicroRNA‐210 (miR‐210) promotes angiogenesis and neurogenesis in the subventricular zone and hippocampus after cerebral ischemia; however, whether miR‐210 regulates NPC migration and the underlying mechanism is still unclear. This study investigated the role of miR‐210 in NPC migration.Methods and ResultsNeovascularization and NPC accumulation was detected around ischemic foci in a mouse model of middle cerebral artery occlusion (MCAO) and reperfusion. Bone marrow–derived endothelial progenitor cells (EPCs) were found to participate in neovascularization. miR‐210 was markedly upregulated after focal cerebral ischemia/reperfusion. Overexpressed miR‐210 enhanced neovascularization and NPC accumulation around the ischemic lesion and vice versa, strongly suggesting that miR‐210 might be involved in neovascularization and NPC accumulation after focal cerebral ischemia/reperfusion. In vitro experiments were conducted to explore the underlying mechanism. The transwell assay showed that EPCs facilitated NPC migration, which was further promoted by miR‐210 overexpression in EPCs. In addition, miR‐210 facilitated VEGF‐C (vascular endothelial growth factor C) expression both in vitro and in vivo. Moreover, the luciferase reporter assay demonstrated that miR‐210 directly targeted the 3′ untranslated region of SOCS1 (suppressor of cytokine signaling 1), and miR‐210 overexpression in HEK293 cells or EPCs decreased SOCS1 and increased STAT3 (signal transducer and activator of transcription 3) and VEGF‐C expression. When EPCs were simultaneously transfected with miR‐210 mimics and SOCS1, the expression of STAT3 and VEGF‐C was reversed.ConclusionsmiR‐210 promoted neovascularization and NPC migration via the SOCS1–STAT3–VEGF‐C pathway.

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Section: Resultssupporting

confidence: 48%

Section: Stat3-vegf Activation Is Modulated By Mir-210 Through Socs1 mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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MicroRNA‐210 Promotes Accumulation of Neural Precursor Cells Around Ischemic Foci After Cerebral Ischemia by Regulating the SOCS1–STAT3–VEGF‐C Pathway

Meng

Kang

Duan

et al. 2018

JAHA

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“…Overall, data suggest that miR-210 could be used as a therapy, or a therapeutic target for the modulation of angiogenesis in the treatment of ischemic diseases. Indeed, miR-210 has been used as a therapy in vivo to enhance wound healing, and tissue repair, processes in which angiogenesis plays a key role (20). …”

Section: Mir-210 In Vascular Integritymentioning

confidence: 99%

miRNAs in vascular integrity

Cao¹,

Zhang

2017

Experimental and Therapeutic Medicine

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Endothelial cells (ECs) are confirmed as important regulators of vascular integrity, particularly in relation to angiogenesis, wound repair post-injury, and during embryogenesis. Futher, miRNAs have been implicated in EC function and proliferation. Moreover, knockdown of these miRNAs resulted in altered expressions of several important regulators of endothelial biology and angiogenesis including vascular endothelial growth factor receptor 2, endothelial nitric oxide synthase and tubule formation capacity. Several miRNAs have been identified to play a role in the regulation of function, proliferation and growth of vascular ECs. These miRNAs may be important therapeutic targets in the treatment of a range of ischemic diseases, as well as in the regulation of angiogenesis during cancer and tumour progression. The present review discuss some of the important miRNAs having confirmed regulatory role in EC in connection espically with cardiovascular disease.

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Acceleration of healing of the medial collateral ligament of the knee by local administration of synthetic microRNA-210 in a rat model

Sakti

Nakasa

Shoji

et al. 2015

Asia-Pacific Journal of Sports Medicine, Arthroscopy, Rehabilit

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BackgroundInjury to the medial collateral ligament (MCL) of the knee joint is the most common ligament injury of the knee. Ligament healing generally takes a long time. Micro-ribonucleic acid (miRNA) is one of the noncoding RNAs and plays a crucial role in physiological function; miRNA (miR)-210 is known as a potent factor of angiogenesis, which is an important initiator of ligament healing. The purpose of this study is to examine the effect of local injection of double-stranded (ds) miR-210 on the healing of the MCL of rat knee joint.MethodsMCLs of Sprague-Dawley rats were cut transversely. After the fascia and skin were sutured, dsmiR-210 or control dsRNA was injected into the injured site of MCL. At 2 weeks and 4 weeks, histological analysis and immunofluorescence staining of vascular endothelial growth factor, isolectin B4, collagen type 1, and Ki67 as well as a mechanical test were performed. Analysis of complementary deoxyribonucleic acid (cDNA) microarray data was performed at 1 week.ResultsHistological analysis showed that parallel fibres in the injured site were organised at 2 weeks and became thicker at 4 weeks in the miR-210-treated group, whereas the injured site in controls was filled with loose fibrous tissues and was thinner than that in the miR-210-treated group. The number of blood vessels in the miR-210-treated group was significantly higher than that in controls (p < 0.05), and vascular endothelial growth factor, Ki67, and collagen type 1 in the miR-210-treated group were intensely expressed in the repaired site as compared to the control group. The mechanical test indicated that the ultimate failure load in the miR-210-treated group was significantly higher than that in the control group at 2 weeks. The cDNA microarray analysis showed significant upregulation of genes related to cell proliferation and cell differentiation, and genes involved in negative regulation of apoptosis.ConclusionThis study showed that local injection of dsmiR-210 could accelerate MCL healing in rat, which is likely due to stimulation of angiogenesis at the healing site.

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The effect of administration of double stranded MicroRNA-210 on acceleration of Achilles tendon healing in a rat model

Cited by 27 publications

References 28 publications

MicroRNA‐210 Promotes Accumulation of Neural Precursor Cells Around Ischemic Foci After Cerebral Ischemia by Regulating the SOCS1–STAT3–VEGF‐C Pathway

MicroRNA‐210 Promotes Accumulation of Neural Precursor Cells Around Ischemic Foci After Cerebral Ischemia by Regulating the SOCS1–STAT3–VEGF‐C Pathway

miRNAs in vascular integrity

Acceleration of healing of the medial collateral ligament of the knee by local administration of synthetic microRNA-210 in a rat model

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