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Promoter Capture Hi-C: High-resolution, Genome-wide Profiling of Promoter Interactions
Published on: June 28, 2018
[Promoter effect induced by HgCl2 by studying the intercellular communication]
M Lasalvia1, R Zefferino, C Piccoli
1Dipartimento di Scienze Mediche e del Lavoro, Università di Foggia. m.lasalvia@unifg.it
Giornale Italiano Di Medicina Del Lavoro Ed Ergonomia
|April 16, 2008
Summary
Mercury (HgCl2) at low doses increases connexin expression and reactive oxygen species (ROS) in human keratinocytes, suggesting redox signaling may inactivate gap junctions.
Area of Science:
- Cell Biology
- Toxicology
- Molecular Biology
Background:
- Intercellular communication is vital for skin homeostasis.
- Mercury compounds can disrupt cellular functions.
- Non-cytotoxic doses of mercury may induce subtle molecular changes.
Purpose of the Study:
- To investigate the molecular effects of mercury(II) chloride (HgCl2) on human keratinocytes (HUKE) at non-cytotoxic levels.
- To assess the impact of HgCl2 on connexin expression and reactive oxygen species (ROS) production.
Main Methods:
- Human keratinocytes (HUKE) were exposed to 10 nM HgCl2 for 24 hours.
- Connexin (Cx) protein and mRNA levels (Cx43, Cx32, Cx26) were quantified using Western blotting and RT-PCR.
- Reactive oxygen species (ROS) production was measured using DCF probe and confocal microscopy.
Main Results:
- HgCl2 exposure led to increased mRNA transcripts for Cx26, Cx32, and Cx43.
- Elevated protein levels of Cx43, Cx32, and Cx26 were observed in HgCl2-treated cells.
- A significant increase in ROS production was detected in mitochondria of HgCl2-treated keratinocytes.
Conclusions:
- Non-cytotoxic concentrations of HgCl2 can alter the redox cellular state by increasing ROS levels.
- The observed increase in ROS may be linked to the inactivation of gap junctions.
- Redox signaling pathways might play a role in mediating HgCl2's effects on keratinocyte communication.
