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Updated: Mar 25, 2026
Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
Published on: March 2, 2019
Increased TMEM16A Involved in Alveolar Fluid Clearance After Lipopolysaccharide Stimulation
Honglin Li1, Xixin Yan2, Rongqin Li3
1Department of Respirology, The Second Hospital of Hebei Medical University, No. 215, West Heping Road, Shijiazhuang, Hebei, 050000, China.
Unlabelled:
Transmembrane protein 16A (TMEM16A) regulates a wide variety of cellular activities, including epithelial fluid secretion and maintenance of ion homeostasis. Lipopolysaccharide (LPS), an outer membrane component of Gram-negative bacteria, is one of the major causes of acute lung injury (ALI). In this study, we investigated the effects of LPS on the expression of TMEM16A in LA795 cells and mouse lung tissue and the potential mechanism.
Result:
We detected the expression of TMEM16A in LA795 cells and mouse lung tissue by RT-PCR, Western blot, and RNA interference techniques. TMEM16A expression was significantly increased by LPS stimulation in LA795 cells and in mouse lung tissue. Moreover, the LPS-induced TMEM16A expression enhancement in lung tissue was much more prominent in the alveolar epithelial region than in bigger airway epithelial cells. The typical TMEM16A current was recorded, and LPS treatment significantly enhances the current amplitude in LA795 cells. TMEM16A shRNA or TMEM16A inhibitor (T16Ainh-A01) did not affect alveolar fluid clearance (AFC), while co-application of T16Ainh-A01 induced a stronger AFC inhibition than LPS alone. LPS notably and synchronously enhanced Akt phosphorylation (p-Akt) and TMEM16A expression in a time-dependent manner in LA795 cells. Taken together, our results suggest that TMEM16A maybe plays an important role in pathological conditions of LPS-induced ALI as a protective protein.
Insights
Lipopolysaccharide (LPS) increases transmembrane protein 16A (TMEM16A) expression in lung cells and tissue, suggesting TMEM16A acts protectively in acute lung injury (ALI). Further research is needed to confirm its role.
Area of Science:
- Cellular biology
- Molecular biology
- Physiology
Background:
- Transmembrane protein 16A (TMEM16A) is crucial for epithelial functions like fluid secretion and ion homeostasis.
- Lipopolysaccharide (LPS), from Gram-negative bacteria, is a key factor in acute lung injury (ALI).
Purpose of the Study:
- To investigate LPS effects on TMEM16A expression in LA795 cells and mouse lung tissue.
- To explore the underlying mechanisms of LPS-induced TMEM16A modulation and its role in ALI.
Main Methods:
- Quantitative analysis of TMEM16A expression using RT-PCR and Western blot.
- Functional assessment via RNA interference and electrophysiology.
- Investigation of signaling pathways, including Akt phosphorylation.
Main Results:
- LPS stimulation significantly upregulated TMEM16A expression in both LA795 cells and mouse lung tissue, particularly in alveolar epithelium.
- LPS enhanced TMEM16A-mediated currents in LA795 cells.
- LPS treatment increased Akt phosphorylation and TMEM16A expression concurrently.
Conclusions:
- TMEM16A expression is upregulated by LPS in lung tissues.
- TMEM16A may function as a protective protein in LPS-induced ALI.
- Inhibition of TMEM16A exacerbates LPS-induced alveolar fluid clearance impairment.
