Decreased miR-195 Expression Protects Rats from Spinal Cord Injury Primarily by Targeting HIF-1α
Hypoxia-inducible factor 1-alpha (HIF-1α) protects hypoxic cells from apoptosis and necrosis under ischemic and anoxic conditions. miRNAs are important regulators in the genome. This study aims to explore whether miR-195 is involved in spinal cord injury through HIF-1α. A total of 40 male Sprague-Da...
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Published in | Annals of clinical and laboratory science Vol. 46; no. 1; pp. 49 - 53 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
United States
2016
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Subjects | |
Online Access | Get full text |
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Summary: | Hypoxia-inducible factor 1-alpha (HIF-1α) protects hypoxic cells from apoptosis and necrosis under ischemic and anoxic conditions. miRNAs are important regulators in the genome. This study aims to explore whether miR-195 is involved in spinal cord injury through HIF-1α. A total of 40 male Sprague-Dawley (SD) rats were separated into four groups: Sham, Control, Ad-con, and Ad-miR-195. The behavior recovery was explored using the Basso, Beattie and Bresnahan (BBB) scoring system. Then, the rats were sacrificed, and the spinal cords were collected. The levels of the HIF-1α, Bcl-2, Bax and VEGF proteins were explored using western blotting. H&E and immunohistochemistry were applied to study the morphological changes. qPCR analysis revealed that miR-195 was significantly decreased after spinal cord injury (SCI). Meanwhile, the expression of Bcl-2, VEGF and HIF-1α was increased in animals after SCI. More importantly, administration with Ad-miR-195 significantly decreased the HIF-1α protein level, thereby reducing Bcl-2 and VEGF expression. In addition, Ad-miR-195 also obviously increased the number of apoptotic cells and decreased the neurological recovery in the animals injected with Ad-miR-195. In conclusion, reduced miR-195 expression partially protects rats from spinal cord injury, primarily by targeting HIF-1α. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1550-8080 |