Effects of MAL gene knockout on lung tissue morphology and on E-cad and α-SMA expression in asthma mouse models

Abstract

Objectives

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.

Methods

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.

Results

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).

Conclusions

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.

Keywords:

• MAL gene knockout
• asthma
• airway remodeling
• E-cad
• α-SMA

Acknowledgments

We gratefully acknowledge Hunan Slac Jingda Experimental Animal Co., Ltd. for providing C57BL/6J wild-type mice and GemPharmatech Co., Ltd. for providing MAL gene knockout (MAL-/-) mice.

Disclosure statement

The authors report there are no competing interests to declare.

Data availability statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Additional information

Funding

This work was supported by the General Program of National Natural Science Foundation of China #1 under Grant number 81873282; Clinical Research 4310 Program of the Frist Affiliated Hospital of the University of South China #2 under Grant number 20214310NHYCG04.