关键词: E-cad MAL gene knockout airway remodeling asthma α-SMA

来  源:   DOI:10.1080/02770903.2024.2355982

Abstract:
UNASSIGNED: To investigate the effects of myelin- and lymphocyte-associated protein (MAL) gene knockout on the morphological structure of lung tissue and the expression of E-cadherin (E-cad) and alpha-smooth muscle actin (α-SMA) in an asthmatic mouse model.
UNASSIGNED: Twenty-four specific pathogen-free (SPF) C57BL/6J mice were divided into four groups: the wild-type normal (WT/SAL), wild-type asthmatic (WT/OVA), gene knockout normal (MAL-/-/SAL), and gene knockout asthmatic (MAL-/-/OVA) groups. The establishment of the asthma mouse models was confirmed by evaluating behavioral symptoms and histopathological H&E and Masson staining. Western blotting and RT-qPCR were used to measure E-cad and α-SMA expression levels in lung tissues.
UNASSIGNED: H&E staining of mouse lung tissues from WT/OVA, MAL-/-/SAL, and MAL-/-/OVA groups revealed a thickened bronchial wall, irregular lumen edge, locally fallen mucosal epithelium, and inflammatory cell infiltration compared with those of the WT/SAL group. In the WT and MAL-/- groups, the proportion of Masson-stained tissues in the OVA group was greater than that in the SAL group (p < 0.05). Compared with those in the WT/SAL group, the expression levels of α-SMA mRNA and protein were increased, while those of E-cad were decreased in the WT/OVA group (p < 0.01). Similarly, compared with those in the MAL-/-/SAL group, the expression levels of E-cad mRNA and protein were increased, while those of α-SMA were decreased in the MAL-/-/OVA group (p < 0.01). All these differences were statistically significant (p < 0.01).
UNASSIGNED: The MAL gene contributes to EMT inhibition and the stability of the airway barrier under normal physiological conditions by regulating E-cad and α-SMA expression.
摘要:
研究骨髓和淋巴细胞相关蛋白(MAL)基因敲除对哮喘小鼠模型肺组织形态结构和E-cadherin(E-cad)和α-平滑肌肌动蛋白(α-SMA)表达的影响。
将24只无特定病原体(SPF)C57BL/6J小鼠分为四组:野生型正常(WT/SAL),野生型哮喘(WT/OVA),基因敲除正常(MAL-/-/SAL),和基因敲除哮喘(MAL-/-/OVA)组。通过评估行为症状和组织病理学H&E和Masson染色证实哮喘小鼠模型的建立。免疫印迹和RT-qPCR检测肺组织中E-cad和α-SMA的表达水平。
WT/OVA小鼠肺组织的H&E染色,MAL-/-/SAL,MAL-/-/OVA组显示支气管壁增厚,不规则的管腔边缘,局部脱落的粘膜上皮,与WT/SAL组相比,炎症细胞浸润。在WT和MAL-/-组中,OVA组Masson染色组织的比例大于SAL组(p<0.05)。与WT/SAL组相比,α-SMAmRNA和蛋白表达水平升高,WT/OVA组E-cad降低(p<0.01)。同样,与MAL-/-/SAL组相比,E-cadmRNA和蛋白表达水平升高,而MAL-/-/OVA组的α-SMA降低(p<0.01)。所有这些差异均具有统计学意义(p<0.01)。
MAL基因通过调节E-cad和α-SMA表达,有助于EMT抑制和正常生理条件下气道屏障的稳定性。
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