Hpgds-KO Mouse

Hpgds, known as 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 physiological and pathological processes [1,2,5,6]. Hpgds has shown importance in multiple biological functions and disease contexts, making it a gene of interest for understanding disease mechanisms and potential therapeutic targets.

In type 2 diabetic mice, Hpgds was significantly down-regulated in wound tissues, and its deficiency delayed normal wound healing. Overexpressing Hpgds in adipose-derived mesenchymal stem cells (ADSC) 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 invasion, suggesting its role in regulating lipid metabolism and tumor aggressiveness in lung adenocarcinoma [2]. In small ruminants, miR-665 overexpression inhibited luteal cell apoptosis by suppressing Hpgds, indicating its involvement in luteal cell apoptosis regulation [3]. In Ashidan yaks, the copy number variation of Hpgds gene was significantly correlated with growth traits such as body weight and body length [4].

In conclusion, Hpgds plays essential roles in processes like wound healing, lipid metabolism, luteal cell apoptosis, and growth trait regulation in different species. Gene-targeted mouse models and other functional studies have provided valuable insights into its role in diseases such as diabetes-related wound healing and lung adenocarcinoma development. Understanding Hpgds can potentially contribute to developing new therapeutic strategies for these diseases.

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/