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Current Molecular Medicine
Current Molecular Medicine
Tuesday, November 1, 2016
Highlighted Article: High-Dose Linoleic Acid Activated JAK2-STAT3 Signaling Pathway Involved in Cytokine Production and Lipogenesis in Pancreatic Exocrine Cells
High-Dose Linoleic Acid Activated JAK2-STAT3 Signaling Pathway Involved in Cytokine Production and Lipogenesis in Pancreatic Exocrine Cells
Author(s):
F. Zhu, Y. Guan and R. Zhang Pages 668 - 676 ( 9 )
Abstract:
Background: Linoleic acid has been implicated in the pathogenesis of acute pancreatitis. However, molecular mechanisms underlying adverse effects of large-dose linoleic acid remain unclear. Current study aimed to explore the impact of high-dose linoleic acid on the activation of Janus kinase 2 (JAK2)-signal transducers and activators of transcription 3 (STAT3) pathway, cytokine production, and lipogenesis in pancreatic exocrine cells.
Methods: MTT assay was used to detect the viability of AR42J rat pancreatic exocrine cells, and lactate dehydrogenase assay was utilized to detect cytotoxicity. Concentrations of interleukin (IL)-6 and tumor necrosis factor (TNF)-α were detected by ELISA, and protein expression of JAK2, p-JAK2, STAT3, p- STAT3, and fatty acid synthase (FAS) was examined by Western Blot. The impact of highdose linoleic acid on JAK2-STAT3 pathway was also examined when JAK2 was inhibited by AG490, and STAT3 expression was interrupted by siRNA.
Results: The cell viability of AR42J rat pancreatic exocrine cells was inhibited, and cytotoxicity was increased by high-dose linoleic acid. JAK2 and STAT3 proteins in pancreatic exocrine cells were activated by high-dose linoleic acid via phosphorylation and nuclear localization of phosphorylated STAT3. Moreover, the expression of downstream proteins in JAK2-STAT3 pathway (IL-6, TNF-α and FAS) was up-regulated by high-dose linoleic acid. The increased levels of IL-6 and TNF-α caused by high-dose linoleic acid were attenuated by JAK2 inhibitor AG490. p-JAK2 protein was up-regulated, whereas p-STAT3, STAT3 and FAS proteins were down-regulated by high-dose linoleic acid in the presence of STAT3-siRNA.
Conclusion: The cytotoxicity was increased and JAK2-STAT3 signaling pathway was activated by high-dose linoleic acid through cytokine production and lipogenesis in rat pancreatic exocrine cells.
Keywords:
JAK2, STAT3, linoleic acid, cytokines, fatty acid synthase.
Affiliation:
Department of Gastroenterology, Shanghai East Hospital, Shanghai Tongji University School of Medicine, No. 150 Jimo Road, Pudong New District, Shanghai 200120, China.
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Monday, October 24, 2016
Most Cited Article: Emerging Role for αB-Crystallin as a Therapeutic Agent: Pros and Cons
Emerging Role for
αB-Crystallin as a Therapeutic Agent: Pros and Cons
Author(s):
V.S. Reddy and G.B. ReddyPages 47-61 (15)
Abstract:
HSPB5 or αB-crystallin (αBC) is a major protein of the vertebrate eye lens belonging to the small heat-shock protein family of proteins that respond to various stressful conditions. αBC also is found outside the lens in various non-ocular tissues and acts as a molecular chaperone by preventing aggregation of proteins, inhibits apoptosis and inflammation, and maintains cytoskeletal architecture. The αBC protein is phosphorylated on three serine residues S59, S45, and S19, and several functions of αBC are modulated by phosphorylation. Numerous studies have revealed the upregulation of αBC in pathological conditions such as neurodegenerative diseases, cancers, diabetes, retinal diseases, cataracts, ischemia/repurfusion, aging, and others. However, it is unknown whether the up-regulation of αBC is causative or protective for these pathological conditions. Although αBC has been shown to provide a protective effect in neurodegenerative diseases, inflammation, diabetes, and retinal diseases, other studies have described a deleterious role of αBC in cancers and pulmonary fibrosis. The therapeutic potential of αBC alone or in combination with αA-crystallin has been reported. Acetylated αBC peptides have been shown to be more potent than native αBC for chaperone as well as therapeutic activities using both in vitro and in vivo models. Further, for efficient delivery of α BC into cells, carrier molecules such as polylacticcoglycolic acid, polycaprolactone and cell penetration peptides have been used. In this review, we have summarized current data from emerging and exciting studies of the therapeutic strategies of α BC and α BC peptides and the efficient delivery strategies of these proteins in various disease models, including neurodegenerative diseases, retinal diseases, platelet aggregation, inflammation, and ischemia.
Keywords:
αB-crystallin, chaperone, stress, disease,
therapeutic activity, peptide.
Affiliation:
National Institute of Nutrition, Hyderabad-500
007, India.
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Tuesday, October 18, 2016
Serum miRNAs Signature Plays an Important Role in Keloid Disease
Article Details
Serum miRNAs Signature Plays an Important Role in Keloid Disease
Author(s):
Y. Luan, Y. Liu, C. Liu, Q. Lin, F. He, X.
Dong and Z. XiaoPages 504-514 (11)
Abstract:
The molecular mechanism underlying the pathogenesis of keloid is largely unknown. MicroRNA (miRNA) is a class of small regulatory RNA that has emerged as a group of posttranscriptional gene repressors, participating in diverse pathophysiological processes of skin diseases. We investigated the expression profiles of miRNAs in the sera of patients to decipher the complicated factors involved in the development of keloid disease. MiRNA expression profiling in the sera from 9 keloid patients and 7 normal controls were characterized using a miRNA microarray containing established human mature and precursor miRNA sequences. Quantitative real-time PCR was performed to confirm the expression of miRNAs. The putative targets of differentially expressed miRNAs were functionally annotated by bioinformatics. MiRNA microarray analysis identified 37 differentially expressed miRNAs (17 upregulated and 20 downregulated) in keloid patients, compared to the healthy controls. Functional annotations revealed that the targets of those differentially expressed miRNAs were enriched in signaling pathways essential for scar formation and wound healing. The expression profiling of miRNAs is altered in the keloid, providing a clue for the molecular mechanisms underlying its initiation and progression. MiRNAs may partly contribute to the etiology of keloids by affecting the critical signaling pathways relevant to keloid pathogenesis.
Keywords:
Keloid, microRNA, serum, pathogenesis, scar,
etiology.
Affiliation:
BRC1217C, Stanton L. Young Biomedical Research
Center, 975 NE 10th St., Oklahoma City, OK 73104, USA., Department of Plastic
and Aesthetic, The Second Affiliated Hospital of Harbin Medical University,
Harbin 150086, People’s Republic of China.
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