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ABCA1 deficiency disrupts the junctional integrity of the colonic mucosal barrier. (A) Representative images of immunofluorescence staining of the zippering junction with <t>E‐cadherin.</t> (B, C) Effects of ABCA1 silencing on cholesterol crystals (CHO)‐induced cell injury. Caco‐2 cells were transfected with siNC or siABCA1 for 24 h, and then exposed to 1 mmol/L CHO or not for 24 h. The cell viability was determined using Calcein‐AM/PI staining (B) and CCK8 assay (C). The data in panel C are expressed as mean ± SD ( n = 4; *** p < 0.001 vs . siNC without CHO by Student's t ‐test). (D) ABCA1 silencing aggravates CHO‐mediated barrier dysfunction in Caco‐2 cells. Caco‐2 cells were transfected with siNC or siABCA1 for 24 h, and then exposed to 1 mmol/L CHO for 6 h. Cellular lysates were assayed for E‐cadherin, Occludin and ZO‐1 expression. The respective densitometric quantitations of bands are presented in the bar graphs to the right of the blots. Data are expressed as mean ± SD ( n = 3; * p < 0.05, ** p < 0.01, *** p < 0.001 vs . siNC without CHO by Student's t ‐test).
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ABCA1 deficiency disrupts the junctional integrity of the colonic mucosal barrier. (A) Representative images of immunofluorescence staining of the zippering junction with <t>E‐cadherin.</t> (B, C) Effects of ABCA1 silencing on cholesterol crystals (CHO)‐induced cell injury. Caco‐2 cells were transfected with siNC or siABCA1 for 24 h, and then exposed to 1 mmol/L CHO or not for 24 h. The cell viability was determined using Calcein‐AM/PI staining (B) and CCK8 assay (C). The data in panel C are expressed as mean ± SD ( n = 4; *** p < 0.001 vs . siNC without CHO by Student's t ‐test). (D) ABCA1 silencing aggravates CHO‐mediated barrier dysfunction in Caco‐2 cells. Caco‐2 cells were transfected with siNC or siABCA1 for 24 h, and then exposed to 1 mmol/L CHO for 6 h. Cellular lysates were assayed for E‐cadherin, Occludin and ZO‐1 expression. The respective densitometric quantitations of bands are presented in the bar graphs to the right of the blots. Data are expressed as mean ± SD ( n = 3; * p < 0.05, ** p < 0.01, *** p < 0.001 vs . siNC without CHO by Student's t ‐test).
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Image Search Results


ABCA1 deficiency disrupts the junctional integrity of the colonic mucosal barrier. (A) Representative images of immunofluorescence staining of the zippering junction with E‐cadherin. (B, C) Effects of ABCA1 silencing on cholesterol crystals (CHO)‐induced cell injury. Caco‐2 cells were transfected with siNC or siABCA1 for 24 h, and then exposed to 1 mmol/L CHO or not for 24 h. The cell viability was determined using Calcein‐AM/PI staining (B) and CCK8 assay (C). The data in panel C are expressed as mean ± SD ( n = 4; *** p < 0.001 vs . siNC without CHO by Student's t ‐test). (D) ABCA1 silencing aggravates CHO‐mediated barrier dysfunction in Caco‐2 cells. Caco‐2 cells were transfected with siNC or siABCA1 for 24 h, and then exposed to 1 mmol/L CHO for 6 h. Cellular lysates were assayed for E‐cadherin, Occludin and ZO‐1 expression. The respective densitometric quantitations of bands are presented in the bar graphs to the right of the blots. Data are expressed as mean ± SD ( n = 3; * p < 0.05, ** p < 0.01, *** p < 0.001 vs . siNC without CHO by Student's t ‐test).

Journal: Animal Models and Experimental Medicine

Article Title: ABCA1 deficiency‐induced cholesterol accumulation aggravates colonic epithelial injury in knockout hamsters

doi: 10.1002/ame2.70301

Figure Lengend Snippet: ABCA1 deficiency disrupts the junctional integrity of the colonic mucosal barrier. (A) Representative images of immunofluorescence staining of the zippering junction with E‐cadherin. (B, C) Effects of ABCA1 silencing on cholesterol crystals (CHO)‐induced cell injury. Caco‐2 cells were transfected with siNC or siABCA1 for 24 h, and then exposed to 1 mmol/L CHO or not for 24 h. The cell viability was determined using Calcein‐AM/PI staining (B) and CCK8 assay (C). The data in panel C are expressed as mean ± SD ( n = 4; *** p < 0.001 vs . siNC without CHO by Student's t ‐test). (D) ABCA1 silencing aggravates CHO‐mediated barrier dysfunction in Caco‐2 cells. Caco‐2 cells were transfected with siNC or siABCA1 for 24 h, and then exposed to 1 mmol/L CHO for 6 h. Cellular lysates were assayed for E‐cadherin, Occludin and ZO‐1 expression. The respective densitometric quantitations of bands are presented in the bar graphs to the right of the blots. Data are expressed as mean ± SD ( n = 3; * p < 0.05, ** p < 0.01, *** p < 0.001 vs . siNC without CHO by Student's t ‐test).

Article Snippet: Then, proteins were transferred to a polyvinylidene difluoride membrane and hybridized with the following antibodies: ABCA1 (26564‐1‐AP, Proteintech, Wuhan, China), ABCA1 (96292, Cell Signaling Technology, Danvers, MA), ZO‐1 (A0659, ABclonal, Wuhan, China), E‐cadherin (sc‐8426, Santa cruz Biotechnology, Santa Cruz, CA), Occludin (66378‐1‐Ig, Proteintech, Wuhan, China), p‐p38 (8796‐1‐AP, Proteintech, Wuhan, China) or β‐actin (66009‐1‐Ig, Proteintech, Wuhan, China).

Techniques: Immunofluorescence, Staining, Transfection, CCK-8 Assay, Expressing