Hpgds-KO Mouse

Hpgds, short for hematopoietic prostaglandin D synthase, is responsible for the production of prostaglandin D2 (PGD2), an inflammatory mediator. It is involved in the arachidonic acid metabolism pathway, which is crucial for various biological processes related to inflammation, lipid metabolism, and cell-cell signaling [1,2,5,6]. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, can be valuable for studying its functions.

In a type 2 diabetic mouse model, Hpgds was significantly down-regulated in the wound area, and its deficiency delayed normal wound healing. Overexpressing Hpgds in adipose-derived mesenchymal stem cells (ADSCs) accelerated diabetic wound healing by reducing neutrophil and CD8T cell recruitment, promoting M2 macrophage polarization, and increasing growth factor production [1]. In A549 cell lines, knockdown of Hpgds promoted lipid synthesis and cell migration, suggesting its role in lipid metabolism and cancer cell invasion in lung adenocarcinoma [2]. In small ruminants, miR-665 overexpression inhibited luteal cell apoptosis by suppressing Hpgds, indicating its involvement in luteal cell regulation [3]. In Ashidan yaks, the copy number variation of the Hpgds gene was associated with growth traits, such as body weight and body length [4].

In conclusion, Hpgds plays essential roles in wound healing, lipid metabolism, luteal cell apoptosis regulation, and growth trait determination in different species. The use of gene knockout mouse models in these studies has revealed its significance in various disease-related and physiological processes, including diabetes-related wound healing, lung adenocarcinoma development, and luteolysis regulation, providing potential therapeutic targets for these conditions.

References:

1. Ouyang, Long, Qiu, Daojing, Fu, Xin, Yan, Li, Xiao, Ran. 2022. Overexpressing HPGDS in adipose-derived mesenchymal stem cells reduces inflammatory state and improves wound healing in type 2 diabetic mice. In Stem cell research & therapy, 13, 395. doi:10.1186/s13287-022-03082-w. https://pubmed.ncbi.nlm.nih.gov/35922870/

2. Shao, Fengling, Mao, Huajie, Luo, Tengling, Xu, Lei, Xie, Yajun. 2022. HPGDS is a novel prognostic marker associated with lipid metabolism and aggressiveness in lung adenocarcinoma. In Frontiers in oncology, 12, 894485. doi:10.3389/fonc.2022.894485. https://pubmed.ncbi.nlm.nih.gov/36324576/

3. Yang, Heng, Fu, Lin, Li, Licai, Li, Qianyong, Zhou, Peng. 2023. miR-665 overexpression inhibits the apoptosis of luteal cells in small ruminants suppressing HPGDS. In Theriogenology, 206, 40-48. doi:10.1016/j.theriogenology.2023.04.027. https://pubmed.ncbi.nlm.nih.gov/37178673/

4. Huang, Chun, Ge, Fei, Ren, Wenwen, Yan, Ping, Liang, Chunnian. 2020. Copy number variation of the HPGDS gene in the Ashidan yak and its associations with growth traits. In Gene, 772, 145382. doi:10.1016/j.gene.2020.145382. https://pubmed.ncbi.nlm.nih.gov/33373661/

5. Chiba, Yoshihiko, Suto, Wataru, Sakai, Hiroyasu. 2018. Augmented Pla2g4c/Ptgs2/Hpgds axis in bronchial smooth muscle tissues of experimental asthma. In PloS one, 13, e0202623. doi:10.1371/journal.pone.0202623. https://pubmed.ncbi.nlm.nih.gov/30161143/

6. Liu, Yong, Liang, Youcheng, Su, Yongjian, Zheng, Mingbin, Huang, Zunnan. 2023. Exploring the potential mechanisms of Yi-Yi-Fu-Zi-Bai-Jiang-San therapy on the immune-inflamed phenotype of colorectal cancer via combined network pharmacology and bioinformatics analyses. In Computers in biology and medicine, 166, 107432. doi:10.1016/j.compbiomed.2023.107432. https://pubmed.ncbi.nlm.nih.gov/37729701/