Hsa-miR-15b-5p/miR-195-5p Controls Osteogenic Differentiation of Human Adipose-Derived Mesenchymal Stem Cells Through Regulating Indian Hedgehog Expression

Harimi, Samaneh; Khansarinejad, Behzad; Fesahat, Farzaneh; Mondanizadeh, Mahdieh

doi:10.1007/s12010-023-04777-3

Cited by 1 publication

(1 citation statement)

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“…Under cyclic tension strain, overexpression of miR-195-5p can significantly inhibit the differentiation of lung adenocarcinoma by targeting WNT family member 3A (Wnt3A) and bone morphogenetic protein receptor 1a (BMPR1A), whereas functional inhibition of miR-195-5p has the opposite effect (43). Hsa-miR-15b-5p/miR-195-5p controls osteogenic differentiation of human adipose-derived mesenchymal stem cells through regulating Indian hedgehog expression (44). These results indicate that miR-195-5p could participate in inhibiting the differentiation of different cell types by targeting multiple genes.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-195-5p targets neurofibromin 2 to mediate hyperoxia-induced alveolar dysplasia

Bai,

Wu,

Yang

et al. 2024

Preprint

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MicroRNAs (miRs) have been shown to disrupt normal lung development and function by blocking alveolation and vascularization, leading to the development of bronchopulmonary dysplasia (BPD). However, the role of miR-195-5p in BPD has not been reported. Therefore, this study aimed to understand whether the biological role of miR-195-5p in BPD is achieved by targeting neurofibromin 2 (NF2) regulation. Here, we report that miR-195-5p plays a key role in hyperoxia-induced alveolar dysplasia in BPD. First, increased expression of miR-195-5p was detected in the lung tissues of hyperoxia-induced rat models of BPD and neonatal rat lung type II alveolar epithelial cells (AECIIs) exposed to hyperoxic conditions. Second, NF2, a tumor suppressor gene that plays an important role in the proliferation and differentiation of AECIIs, was identified as the specific target of miR-195-5p. Cell-based luciferase analysis revealed that the overexpression of miR-195-5p and its target gene NF2 in lung AECIIs could partially alleviate the impaired differentiation of AECIIs induced by hyperoxia, suggesting that miR-195-5p could hinder the differentiation of AECII into AECI by inhibiting NF2 expression. Finally, animal intervention experiments confirmed that miR-195-5p aggravated alveolar dysplasia in BPD by downregulating NF2 expression. In conclusion, our study confirmed a novel mechanism wherein miR-195-5p exacerbates alveolar dysplasia in BPD by inhibiting AECII differentiation to AECI by targeting NF2. These results may help clarify some molecular mechanisms of the poor proliferation and differentiation of AECII in BPD alveolar dysplasia and provide novel targets for future clinical molecular interventions.

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Section: Discussionmentioning

confidence: 99%