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Quantifying cell behaviors in negative-pressure induced monolayer cell movement
Shu-Er Chow1, Carl Pai-Chu Chen2, Chih-Chin Hsu3
1Department of Nature Science, Center for General Studies, Chang Gung University, Taoyuan, Taiwan.
Biomedical Journal
|April 24, 2016
Summary
Negative-pressure (NP) wound therapy enhances keratinocyte migration by altering cell-substrate adhesion and cell-cell junctions. These cellular changes quantified by ECIS may accelerate wound healing.
Area of Science:
- Biomedical Engineering
- Wound Healing Research
- Cell Biology
Background:
- Negative-pressure (NP) therapy, at 125 mmHg, is known to accelerate wound healing.
- This study investigates the specific effects of NP on human keratinocyte behavior during wound healing.
Purpose of the Study:
- To quantify the impact of NP on human keratinocyte migration and cellular dynamics.
- To elucidate the mechanisms by which NP influences cell-substrate and cell-cell interactions.
Main Methods:
- An NP incubator integrated with electric cell-substrate impedance sensing (ECIS) was developed.
- ECIS continuously monitored keratinocyte movement and quantified membrane capacitance (Cm), cell-substratum resistance (α), and cell-cell junction resistance (Rb) under ambient pressure (AP) and NP conditions.
Main Results:
- NP significantly increased keratinocyte migration distance compared to AP.
- NP led to decreased cell-substratum adhesion (lower α), reduced integrin expression, and increased cell-substratum distance.
- NP induced increased membrane ruffling and microtubule formation (higher Cm) and decreased cell-cell junction resistance (lower Rb) with reduced E-cadherin expression.
Conclusions:
- NP promotes rapid membrane ruffling and early cell-substratum separation.
- NP treatment results in decreased intercellular communication.
- These quantified cellular behaviors under NP conditions are proposed mechanisms for accelerated wound healing.
