Over-expression of Spock2 in mice leads to altered lung alveolar development and worsens lesions induced by hyperoxia.

This study brings strong arguments for the deleterious role of SPOCK2 on lung alveolar development especially after lung injury, suggesting its role in BPD susceptibility. These effects are not mediated by a deregulation in metalloproteases activity and in expression of factors essential to normal alveolarization. The balance between type 1 and 2 epithelial alveolar cells may be involved. PMID: 32374670 [PubMed - as supplied by publisher]

https://www.ncbi.nlm.nih.gov/pubmed/32374670?dopt=Abstract

Source: American Journal of Physiology. Lung Cellular and Molecular Physiology - May 5, 2020 Category: Cytology Authors: Hadchouel A, Franco-Montoya ML, Guerin S, Do Cruzeiro M, Lhuillier M, Ribeiro Baptista B, Boyer L, Lanone S, Delacourt C Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research