Hao Zhang1, Wei Liu2, Hongliang Ge3, Kun Li4. 1. The First Department of Neurology, Rizhao People's Hospital, Rizhao, 276800, Shandong, China. 2. Department of Neurology, Zhucheng People's Hospital, Zhucheng, 262200, Shandong, China. 3. Department of Neurology, Shanxian Central Hospital, Heze, 274300, Shandong, China. 4. Department of Neurology, Shanxian Central Hospital, Heze, 274300, Shandong, China. Electronic address: likun_kl@163.com.
Abstract
OBJECTIVE: The current study investigated the expression change and clinical value of miR-148a-3p in AD patients, and further examined the role of miR-148a-3p in Aβ-induced neurotoxicity in SH-SY5Y cells. MATERIAL AND METHODS: qRT-PCR was used for the measurement of miR-148a-3p expression levels. ROC curve was established to calculate the diagnostic value of serum miR-148a-3p for AD. CCK-8 and flow cytometry assay was applied for the detection of cell viability and apoptosis. Additionally, the luciferase reporter assay was performed to confirm the target relationship between ROCK1 and miR-148a-3p. RESULTS: Serum miR-148a-3p was downregulated in AD patients compared with that in healthy controls, and was positively associated with the MMSE score in AD patients. Serum miR-148a-3p had the potential to distinguish AD patients from healthy controls, and the diagnostic sensitivity and specificity were respectively 85.5 % and 87.0 % at a cutoff value of 0.827. MiR-148a-3p attenuated Aβ25-35 induced neurotoxicity in SH-SY5Y cells, and ROCK1 was the target gene. CONCLUSION: Serum miR-148a-3p is correlated with MMSE score in AD patients, and it might be helpful for the AD diagnosis. Overexpression of miR-148a-3p attenuated Aβ induced neurotoxicity in AD by targeting ROCK1.
OBJECTIVE: The current study investigated the expression change and clinical value of miR-148a-3p in AD patients, and further examined the role of miR-148a-3p in Aβ-induced neurotoxicity in SH-SY5Y cells. MATERIAL AND METHODS: qRT-PCR was used for the measurement of miR-148a-3p expression levels. ROC curve was established to calculate the diagnostic value of serum miR-148a-3p for AD. CCK-8 and flow cytometry assay was applied for the detection of cell viability and apoptosis. Additionally, the luciferase reporter assay was performed to confirm the target relationship between ROCK1 and miR-148a-3p. RESULTS: Serum miR-148a-3p was downregulated in AD patients compared with that in healthy controls, and was positively associated with the MMSE score in AD patients. Serum miR-148a-3p had the potential to distinguish AD patients from healthy controls, and the diagnostic sensitivity and specificity were respectively 85.5 % and 87.0 % at a cutoff value of 0.827. MiR-148a-3p attenuated Aβ25-35 induced neurotoxicity in SH-SY5Y cells, and ROCK1 was the target gene. CONCLUSION: Serum miR-148a-3p is correlated with MMSE score in AD patients, and it might be helpful for the AD diagnosis. Overexpression of miR-148a-3p attenuated Aβ induced neurotoxicity in AD by targeting ROCK1.