Jing C. Zhou
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Jing C. Zhou has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Beiyun Zhou
Hastings Center for Pulmonary Research, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA
1 shared publication - Changgong Li
Department of Pediatrics, Women's and Children's Hospital, USC Keck School of Medicine, Los Angeles, CA 90033, USA
1 shared publication - Hongqiao Zhang
Norris Comprehensive Cancer Center, Hastings Center for Pulmonary Research, Department of Molecular Microbiology and Immunology, University of Southern California Keck School of Medicine
1 shared publication - Jason Shin Chwa
Keck School of Medicine University of Southern California Los Angeles California USA
1 shared publication - Parviz Minoo
Division of Neonatology, Department of Pediatrics, University of Southern California
1 shared publication - Rutuja Kibe
Division of Neonatology, Departments of Pediatrics, LAC + USC Medical Center and Children’s Hospital, Los Angeles, CA 90033, USA
1 shared publication
Latest Publications
- Open Access
AKT Signaling Differentially Regulates the Expression of Two Evolutionarily Conserved Wnt5a Isoforms in Lung Mesenchymal Cells
WNT5a is a lipid-modified glycoprotein member of the WNT family of signaling molecules. Two isoforms of WNT5a have been identified that are conserved across mice and humans. These isoforms display specific functions in regulating cancer cell activities. While WNT5a is, indeed, essential for normal lung development and homeostasis, and is dysregulated in multiple lung diseases, little to no information is available regarding the expression or potential function of WNT5a isoforms in normal or diseased lungs. Such information has the potential to help to elucidate the more precise and nuanced functions of WNT5a in various pulmonary conditions. In this study, we characterized the expression of individual Wnt5a isoforms during mouse lung development and compared their expression across major alveolar cell populations. We further investigated the molecular basis of the signaling mechanisms that regulate Wnt5a isoform expression in fibroblasts, the major lung cell type with high-level Wnt5a expression. We present data that reveal a role for the AKT pathway in differentially regulating the expression of Wnt5a isoforms, a novel finding. Furthermore, we demonstrate that Wnt5a isoforms are dysregulated in bleomycin-induced fibrosis and Pseudomonas aeruginosa (PA)-induced acute lung injury and exhibit distinct impacts in Wnt5a isoform expression in response to lung injury.
Open AccessAKT Signaling Differentially Regulates the Expression of Two Evolutionarily Conserved Wnt5a Isoforms in Lung Mesenchymal Cells
WNT5a is a lipid-modified glycoprotein member of the WNT family of signaling molecules. Two isoforms of WNT5a have been identified that are conserved across mice and humans. These isoforms display specific functions in regulating cancer cell activities. While WNT5a is, indeed, essential for normal lung development and homeostasis, and is dysregulated in multiple lung diseases, little to no information is available regarding the expression or potential function of WNT5a isoforms in normal or diseased lungs. Such information has the potential to help to elucidate the more precise and nuanced functions of WNT5a in various pulmonary conditions. In this study, we characterized the expression of individual Wnt5a isoforms during mouse lung development and compared their expression across major alveolar cell populations. We further investigated the molecular basis of the signaling mechanisms that regulate Wnt5a isoform expression in fibroblasts, the major lung cell type with high-level Wnt5a expression. We present data that reveal a role for the AKT pathway in differentially regulating the expression of Wnt5a isoforms, a novel finding. Furthermore, we demonstrate that Wnt5a isoforms are dysregulated in bleomycin-induced fibrosis and Pseudomonas aeruginosa (PA)-induced acute lung injury and exhibit distinct impacts in Wnt5a isoform expression in response to lung injury.