Version 1
: Received: 26 October 2024 / Approved: 26 October 2024 / Online: 28 October 2024 (13:22:59 CET)
How to cite:
Kathuria, I.; Prasad, A.; Sharma, B. K.; Ofosu-Boateng, M.; Aithabathula, R. V.; Gyamfi, M. A.; Jiang, J.; Park, F.; Singh, U. P.; Singla, B. Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis. Preprints2024, 2024102083. https://doi.org/10.20944/preprints202410.2083.v1
Kathuria, I.; Prasad, A.; Sharma, B. K.; Ofosu-Boateng, M.; Aithabathula, R. V.; Gyamfi, M. A.; Jiang, J.; Park, F.; Singh, U. P.; Singla, B. Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis. Preprints 2024, 2024102083. https://doi.org/10.20944/preprints202410.2083.v1
Kathuria, I.; Prasad, A.; Sharma, B. K.; Ofosu-Boateng, M.; Aithabathula, R. V.; Gyamfi, M. A.; Jiang, J.; Park, F.; Singh, U. P.; Singla, B. Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis. Preprints2024, 2024102083. https://doi.org/10.20944/preprints202410.2083.v1
APA Style
Kathuria, I., Prasad, A., Sharma, B. K., Ofosu-Boateng, M., Aithabathula, R. V., Gyamfi, M. A., Jiang, J., Park, F., Singh, U. P., & Singla, B. (2024). Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis. Preprints. https://doi.org/10.20944/preprints202410.2083.v1
Chicago/Turabian Style
Kathuria, I., Udai P. Singh and Bhupesh Singla. 2024 "Nidogen 2 Overexpression Promotes Hepatosteatosis and Atherosclerosis" Preprints. https://doi.org/10.20944/preprints202410.2083.v1
Abstract
The clinical and genetic studies strongly support a significant connection between nonalcoholic fatty liver disease (NAFLD) and atherosclerotic cardiovascular disease (ASCVD) and identify ASCVD as the primary cause of death in NAFLD patients. Understanding the molecular factors and mechanisms regulating these diseases, is critical for developing novel therapies that target them simultaneously. Our preliminary immunoblotting experiments demonstrated elevated expression of nidogen 2 (NID2), a basement membrane glycoprotein, in human atherosclerotic vascular tissues and murine steatotic livers. Therefore, we investigated the role of NID2 in regulating hepatosteatosis and atherosclerosis utilizing Western diet-fed Apoe-/- mice with/without NID2 overexpression. Quantitative real-time PCR confirmed increased NID2 mRNA expression in multiple organs (liver, heart, kidney and adipose) of NID2-overexpressing mice. Male mice with NID2 overexpression exhibited higher liver and epididymal white adipose tissue mass, increased hepatic lipid accumulation and fibrosis. Additionally, these mice developed larger atherosclerotic lesions in the whole aortas and aortic roots, with increased necrotic core formation. Mechanistic studies showed reduced AMPK activation in the livers of NID2-overexpressing mice compared with controls, without any effects on hepatic inflammation. In conclusion, these findings suggest that NID2 plays a deleterious role in both hepatosteatosis and atherosclerosis, making it a potential therapeutic target for these conditions.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
