SavedAdd your journal

Journals / Annals of Medical Research / 2022 / Cilt: 29 - Sayı: 4

The expression levels of genes involved in JNK signaling decrease by aging in the liver

Başak KAYHAN
Elif KAYHAN KUŞTEPE
Gamze KARACA
Zeynel Mete KARACA
Pages
357–362
Publication Date
2022-10-12
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: According to these results, spontaneous liver damage that can be seen in aged subjects may be caused by disruption in cellular signaling pathways and organelle damage in hepatocytes.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Aim: The c-Jun NH2-terminal kinases (JNK) signaling pathway is an important signaling pathway in liver regeneration. it was planned to investigate the expression levels of Mitogen Activated Protein Kinase Kinase (MKK)-4 and -7 (MKK7), which are mediator molecules involved in the JNK signaling pathway and Activating Transcription Factor (ATF) 2 transcription factor genes, which are in the last stage of the signaling pathway, in liver tissues in young and old mice.
📊
Key Findings & Data:Material and Methods: We examined MKK4, MKK7 and ATF2 expression levels by using Real Time Polymerase Chain Reaction (RT-qPCR) method.
💡
Conclusion & Impact:Conclusion: According to these results, spontaneous liver damage that can be seen in aged subjects may be caused by disruption in cellular signaling pathways and organelle damage in hepatocytes.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Aim: The c-Jun NH2-terminal kinases (JNK) signaling pathway is an important signaling pathway in liver regeneration. it was planned to investigate the expression levels of Mitogen Activated Protein Kinase Kinase (MKK)-4 and -7 (MKK7), which are mediator molecules involved in the JNK signaling pathway and Activating Transcription Factor (ATF) 2 transcription factor genes, which are in the last stage of the signaling pathway, in liver tissues in young and old mice. In addition, it was aimed to examine the ultrastructural changes caused by aging in hepatocytes. Material and Methods: We examined MKK4, MKK7 and ATF2 expression levels by using Real Time Polymerase Chain Reaction (RT-qPCR) method. Transmission electron microscopy (TEM) was used to observe the ultrastructural changes of hepatocytes. Results: While MKK4 and ATF2 gene expressions reduced in the liver of aged mice, MKK7 gene expression did not change. In TEM examinations, granular endoplasmic reticulum loss and mitochondrial damage were observed in elderly individuals. Conclusion: According to these results, spontaneous liver damage that can be seen in aged subjects may be caused by disruption in cellular signaling pathways and organelle damage in hepatocytes.

🔖

Cite This Article

KAYHAN, B., KUŞTEPE, E. K., KARACA, G., KARACA, Z. M. (2022). The expression levels of genes involved in JNK signaling decrease by aging in the liver. Annals of Medical Research, Cilt: 29 - Sayı: 4, 357–362. https://ajindex.com/articles/445652

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (18)

  1. Kim IH, Kisseleva T, Brenner DA. Aging and liver disease. Current opinion in gastroenterology. 2015;313:184-91
  2. Michielsen P, Vandewoude M. Liver diseases in the older adult. Acta Gastroenterol Belg. 2010;731:1-4
  3. Carrier P, Debette-Gratien M, Jacques J, Loustaud-Ratti V. Cirrhotic patients and older people. World J Hepatol. 2019;119:663- 77
  4. Schmucker DL, Sanchez H. Liver regeneration and aging: a current perspective. Current gerontology and geriatrics research. 2011;2011:526379-
  5. Durand F, Levitsky J, Cauchy F, et al. Age and liver transplantation. Journal of Hepatology. 2019;704:745-58
  6. Wuestefeld T, Pesic M, Rudalska R, et al. A Direct in vivo RNAi screen identifies MKK4 as a key regulator of liver regeneration. Cell. 2013;1532:389-401
  7. Cargnello M, Roux PP. Activation and function of the MAPKs and their substrates, the MAPK-activated protein kinases. Microbiol Mol Biol Rev. 2011;751:50-83
  8. Lin A. Activation of the JNK signaling pathway: breaking the brake on apoptosis. Bioessays. 2003;251:17-24
  9. Gupta S, Barrett T, Whitmarsh AJ, et al. Selective interaction of JNK protein kinase isoforms with transcription factors. EMBO J. 1996;1511:2760-70
  10. Bode AM, Dong Z. The functional contrariety of JNK. Mol Carcinog. 2007;468:591-8
  11. Kyriakis JM, Banerjee P, Nikolakaki E, et al. The stressactivated protein kinase subfamily of c-Jun kinases. Nature. 1994;3696476:156-60
  12. Fedarko NS. The biology of aging and frailty. Clin Geriatr Med. 2011;271:27-37
  13. Ishigami A, Reed TD, Roth GS. Effect of aging on EGF stimulated DNA synthesis and EGF receptor levels in primary cultured rat hepatocytes. Biochem Biophys Res Commun. 1993;1961:181-6
  14. Atadja PW, Stringer KF, Riabowol KT. Loss of serum response element-binding activity and hyperphosphorylation of serum response factor during cellular aging. Mol Cell Biol. 1994;147:4991- 9
  15. Riabowol K, Schiff J, Gilman MZ. Transcription factor AP-1 activity is required for initiation of DNA synthesis and is lost during cellular aging. Proceedings of the National Academy of Sciences. 1992;891:157-61
  16. Kurtoğlu EL, Kayhan B, Gül M, et al. A bioactive product lipoxin A4 attenuates liver fibrosis in an experimental model by regulating immune response and modulating the expression of regeneration genes. Turk J Gastroenterol. 2019;308:745-57
  17. Kim IH, Kisseleva T, Brenner DA. Aging and liver disease. Curr Opin Gastroenterol. 2015;313:184-91
  18. Kim EK, Choi EJ. Pathological role