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Role of microRNAs in Vascular Remodeling

View Article: PubMed Central - PubMed

ABSTRACT

Besides being involved in the gradual formation of blood vessels during embryonic development, vascular remodeling also contributes to the progression of various cardiovascular diseases, such as; myocardial infarction, heart failure, atherosclerosis, pulmonary artery hypertension, restenosis, aneurysm, etc. The integrated mechanisms; proliferation of medial smooth muscle cell, dysregulation of intimal endothelial cell, activation of adventitial fibroblast, inflammation of macrophage, and the participation of extracellular matrix proteins are important factors in vascular remodeling. In the recent studies, microRNAs (miRs) have been shown to be expressed in all of these cell-types and play important roles in the mechanisms of vascular remodeling. Therefore, some miRs may be involved in prevention and others in the aggravation of the vascular lesions. miRs are small, endogenous, conserved, single-stranded, non-coding RNAs; which degrade target RNAs or inhibit translation post-transcriptionally. In this paper, we reviewed the function and mechanisms of miRs, which are highly expressed in various cells types, especially endothelial and smooth muscle cells, which are closely involved in the process of vascular remodeling. We also assess the functions of these miRs in the hope that they may provide new possibilities of diagnosis and treatment choices for the related diseases.

No MeSH data available.


Related in: MedlinePlus

Modulation of fibrosis or apoptosis by crosstalk of miR-126 and miR-221/222 in endothelial cells. The biogenesis of miR-126 is synthesized by the two transcription factors, ETS-1 and ETS-2 and cofactor, KLF2. miR-126 enhances angiogenesis through the de-regulation of PIK3R2 (the inhibitor of PI3K signaling) or SPRED1 (the inhibitor of ras-raf-MEK-ERK signaling). However, miR-126 enhances angiogenesis through the down-regulation of PIK3R1. Furthermore, miR-126 can inhibit inflammation via targeting VCAM1, which is also down-regulated by miR-221/222. miR-126 can act in an anti-atherosclerosic manner for the release of microparticle containing miR-126 and inhibition of the expression of RGS-16. The RGS-16 down-regulated CXCR4 to increase the expression of CXCL12 and was also down-regulated by miR-126. miR-126 inhibits atherosclerosis growth and recruited progenitor cells to repair the endothelial cells. In addition, miR-221/222 promoted the angiogenesis by targeting STATA5A. Arrows (→) represent up-regulation. Capped lines (┤) indicate inhibition. Abbreviation: chemokine (C-X-C motif) ligand 12 (CXCL12), chemokine (C-X-C motif) receptor 4 (CXCR4), cyclin-dependent kinase inhibitor 1B (p27/Kip1), cyclin-dependent kinase inhibitor 1C (p57/Kip2), E26 transformation-specific sequence-1 (ETS-1), E26 transformation-specific sequence-2 (ETS-2), phosphoinositol-3 kinase (PI3K) regulatory subunit 2 (PIK3R2), regulator of G-protein signaling 16 (RGS16), signal transducer and activator of transcription 5A (STATA5A), sprouty-related protein EVH1 domain containing 1(SPRED1), vascular cell adhesion molecule 1 (VCAM-1).
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Figure 4: Modulation of fibrosis or apoptosis by crosstalk of miR-126 and miR-221/222 in endothelial cells. The biogenesis of miR-126 is synthesized by the two transcription factors, ETS-1 and ETS-2 and cofactor, KLF2. miR-126 enhances angiogenesis through the de-regulation of PIK3R2 (the inhibitor of PI3K signaling) or SPRED1 (the inhibitor of ras-raf-MEK-ERK signaling). However, miR-126 enhances angiogenesis through the down-regulation of PIK3R1. Furthermore, miR-126 can inhibit inflammation via targeting VCAM1, which is also down-regulated by miR-221/222. miR-126 can act in an anti-atherosclerosic manner for the release of microparticle containing miR-126 and inhibition of the expression of RGS-16. The RGS-16 down-regulated CXCR4 to increase the expression of CXCL12 and was also down-regulated by miR-126. miR-126 inhibits atherosclerosis growth and recruited progenitor cells to repair the endothelial cells. In addition, miR-221/222 promoted the angiogenesis by targeting STATA5A. Arrows (→) represent up-regulation. Capped lines (┤) indicate inhibition. Abbreviation: chemokine (C-X-C motif) ligand 12 (CXCL12), chemokine (C-X-C motif) receptor 4 (CXCR4), cyclin-dependent kinase inhibitor 1B (p27/Kip1), cyclin-dependent kinase inhibitor 1C (p57/Kip2), E26 transformation-specific sequence-1 (ETS-1), E26 transformation-specific sequence-2 (ETS-2), phosphoinositol-3 kinase (PI3K) regulatory subunit 2 (PIK3R2), regulator of G-protein signaling 16 (RGS16), signal transducer and activator of transcription 5A (STATA5A), sprouty-related protein EVH1 domain containing 1(SPRED1), vascular cell adhesion molecule 1 (VCAM-1).

Mentions: Up-regulation of CXCL12 inhibited atherosclerosis-induced injuries, and CXCL12 could recruit the Sca-1+ progenitor cells into the cell walls to repair the injury [46] (Fig. 4). In summary, miR-126 has the effect of pro-angiogenesis, anti-inflammation, and anti-atherosclerosis. Hence, it is a promising strategy to use the microvehicle-mediated miRs in patients with atherosclerosis [47].


Role of microRNAs in Vascular Remodeling
Modulation of fibrosis or apoptosis by crosstalk of miR-126 and miR-221/222 in endothelial cells. The biogenesis of miR-126 is synthesized by the two transcription factors, ETS-1 and ETS-2 and cofactor, KLF2. miR-126 enhances angiogenesis through the de-regulation of PIK3R2 (the inhibitor of PI3K signaling) or SPRED1 (the inhibitor of ras-raf-MEK-ERK signaling). However, miR-126 enhances angiogenesis through the down-regulation of PIK3R1. Furthermore, miR-126 can inhibit inflammation via targeting VCAM1, which is also down-regulated by miR-221/222. miR-126 can act in an anti-atherosclerosic manner for the release of microparticle containing miR-126 and inhibition of the expression of RGS-16. The RGS-16 down-regulated CXCR4 to increase the expression of CXCL12 and was also down-regulated by miR-126. miR-126 inhibits atherosclerosis growth and recruited progenitor cells to repair the endothelial cells. In addition, miR-221/222 promoted the angiogenesis by targeting STATA5A. Arrows (→) represent up-regulation. Capped lines (┤) indicate inhibition. Abbreviation: chemokine (C-X-C motif) ligand 12 (CXCL12), chemokine (C-X-C motif) receptor 4 (CXCR4), cyclin-dependent kinase inhibitor 1B (p27/Kip1), cyclin-dependent kinase inhibitor 1C (p57/Kip2), E26 transformation-specific sequence-1 (ETS-1), E26 transformation-specific sequence-2 (ETS-2), phosphoinositol-3 kinase (PI3K) regulatory subunit 2 (PIK3R2), regulator of G-protein signaling 16 (RGS16), signal transducer and activator of transcription 5A (STATA5A), sprouty-related protein EVH1 domain containing 1(SPRED1), vascular cell adhesion molecule 1 (VCAM-1).
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Figure 4: Modulation of fibrosis or apoptosis by crosstalk of miR-126 and miR-221/222 in endothelial cells. The biogenesis of miR-126 is synthesized by the two transcription factors, ETS-1 and ETS-2 and cofactor, KLF2. miR-126 enhances angiogenesis through the de-regulation of PIK3R2 (the inhibitor of PI3K signaling) or SPRED1 (the inhibitor of ras-raf-MEK-ERK signaling). However, miR-126 enhances angiogenesis through the down-regulation of PIK3R1. Furthermore, miR-126 can inhibit inflammation via targeting VCAM1, which is also down-regulated by miR-221/222. miR-126 can act in an anti-atherosclerosic manner for the release of microparticle containing miR-126 and inhibition of the expression of RGS-16. The RGS-16 down-regulated CXCR4 to increase the expression of CXCL12 and was also down-regulated by miR-126. miR-126 inhibits atherosclerosis growth and recruited progenitor cells to repair the endothelial cells. In addition, miR-221/222 promoted the angiogenesis by targeting STATA5A. Arrows (→) represent up-regulation. Capped lines (┤) indicate inhibition. Abbreviation: chemokine (C-X-C motif) ligand 12 (CXCL12), chemokine (C-X-C motif) receptor 4 (CXCR4), cyclin-dependent kinase inhibitor 1B (p27/Kip1), cyclin-dependent kinase inhibitor 1C (p57/Kip2), E26 transformation-specific sequence-1 (ETS-1), E26 transformation-specific sequence-2 (ETS-2), phosphoinositol-3 kinase (PI3K) regulatory subunit 2 (PIK3R2), regulator of G-protein signaling 16 (RGS16), signal transducer and activator of transcription 5A (STATA5A), sprouty-related protein EVH1 domain containing 1(SPRED1), vascular cell adhesion molecule 1 (VCAM-1).
Mentions: Up-regulation of CXCL12 inhibited atherosclerosis-induced injuries, and CXCL12 could recruit the Sca-1+ progenitor cells into the cell walls to repair the injury [46] (Fig. 4). In summary, miR-126 has the effect of pro-angiogenesis, anti-inflammation, and anti-atherosclerosis. Hence, it is a promising strategy to use the microvehicle-mediated miRs in patients with atherosclerosis [47].

View Article: PubMed Central - PubMed

ABSTRACT

Besides being involved in the gradual formation of blood vessels during embryonic development, vascular remodeling also contributes to the progression of various cardiovascular diseases, such as; myocardial infarction, heart failure, atherosclerosis, pulmonary artery hypertension, restenosis, aneurysm, etc. The integrated mechanisms; proliferation of medial smooth muscle cell, dysregulation of intimal endothelial cell, activation of adventitial fibroblast, inflammation of macrophage, and the participation of extracellular matrix proteins are important factors in vascular remodeling. In the recent studies, microRNAs (miRs) have been shown to be expressed in all of these cell-types and play important roles in the mechanisms of vascular remodeling. Therefore, some miRs may be involved in prevention and others in the aggravation of the vascular lesions. miRs are small, endogenous, conserved, single-stranded, non-coding RNAs; which degrade target RNAs or inhibit translation post-transcriptionally. In this paper, we reviewed the function and mechanisms of miRs, which are highly expressed in various cells types, especially endothelial and smooth muscle cells, which are closely involved in the process of vascular remodeling. We also assess the functions of these miRs in the hope that they may provide new possibilities of diagnosis and treatment choices for the related diseases.

No MeSH data available.


Related in: MedlinePlus