Journal: Scientific Reports

Article Title: S100A8 regulated by estrogen improves injured endometrial epithelium reconstruction by promoting tight junction formation and stromal cell transformation

doi: 10.1038/s41598-025-08530-0

Figure Lengend Snippet: Effects of estrogen treatment on S100A8 expression in endometrium and epithelium morphology. ( a ) S100A8 immunohistochemical staining before and after estrogen treatment (1d/7d); black arrows indicate S100A8-positive immune cells (S100A8-PICs).The blue arrow indicates the release of S100A8 from S100A8-PICs. Scale bar is 100 or 400 μm. ( b ) Rat endometrial hematoxylin–eosin staining before and after estrogen treatment (1d/7d); red arrows show disrupted cell junctions. Scale bar is 100 μm. ( c ) S100A8-PICs number in the endometrium (1/mm 2 ) before and 1 d/7d after estrogen treatment (n = 18, from six rats, the number was counted from three immunohistochemical images of each sample , mean ± SEM). ( d ) S100A8 expression in the epithelium before and 1 d/7d after estrogen treatment (n = 18, from six rats, the expression level was measured from three immunohistochemical images of each sample, mean ± SEM). * Results with P values < 0.05 were considered significant. ** Results with P values < 0.01 were considered very significant.

Article Snippet: The cultured cells were randomly divided into three groups according to the experimental design: the control, S100A8 (0.5 μg/mL, HY- P71275 ; MCE, Shanghai, China), and S100A8 + FPS-ZM 1 (5 μM, HY-19370; MCE, Shanghai, China) groups.

Techniques: Expressing, Immunohistochemical staining, Staining

Journal: Scientific Reports

Article Title: S100A8 regulated by estrogen improves injured endometrial epithelium reconstruction by promoting tight junction formation and stromal cell transformation

doi: 10.1038/s41598-025-08530-0

Figure Lengend Snippet: Effects of uterine cavity administration of S100A8 on the distribution of S100A8-PICs and endometrial morphology. ( a ) Distribution of S100A8-positive cells in the endometrium of four different groups with estrogen treatment (control, injury, P407, and S100A8 + P407 groups). Black arrows show S100A8-PICs. S100A8-PICs were distributed around the glands and blood vessels in the control group. S100A8-PICs in the site of injury or adhesion in the injury group and in the P407 group. S100A8-PICs reverse migrated to the glands or blood vessels in the S100A8 + P407 group. Scale bar is 100 μm or 1 mm. ( b ) Endometrial thickness in the four groups (n = 15, from 5 rats; 3 position was measured randomly in an image of each rat, mean ± SEM). ( c ) The number of endometrial glands in each group (n = 10, from 10 rats, glands were counted from a uterine horn cross-section image at 40 × of each rat, mean ± SEM). ( d ) The interior wall integrity of uterine cavity in each group (n = 10, from 10 rats, data was measured from a uterine horn cross-section image at 40 × of each rat, mean ± SEM). ( e ) The number of endometrial crypts in each group (n = 10, from 10 rats, crypts were counted from a uterine horn cross-section image at 40 × of each rat, mean ± SEM). * Results with P values < 0.05 were considered significant. ** Results with P values < 0.01 were considered very significant.

Article Snippet: The cultured cells were randomly divided into three groups according to the experimental design: the control, S100A8 (0.5 μg/mL, HY- P71275 ; MCE, Shanghai, China), and S100A8 + FPS-ZM 1 (5 μM, HY-19370; MCE, Shanghai, China) groups.

Techniques: Control

Journal: Scientific Reports

Article Title: S100A8 regulated by estrogen improves injured endometrial epithelium reconstruction by promoting tight junction formation and stromal cell transformation

doi: 10.1038/s41598-025-08530-0

Figure Lengend Snippet: Effects of S100A8 on the distribution of Ki-67-positive proliferating cells in the uteri and the proliferation of endometrial cells. ( a ) Ki-67-positive proliferating cells were distributed in the endometrium or uterine interior wall in all groups (control, injury, P407, and S100A8 + P407 groups). Scale bar is 100 or 400 μm. ( b ) Number of Ki-67-positive cells in the endometrium of each group (n = 20, from ten rats, the number was counted from two immunohistochemical images of each sample, mean ± SEM). ( c ) Number of Ki-67-positive cells in the uterine interior wall of each group (n = 20, from ten rats, the number was counted from two immunohistochemical images of each sample, mean ± SEM). ( d ) Effects of S100A8 and its receptor inhibitor (FPS-ZM1) on the proliferation of cultured endometrial cells in vitro (n = 5, mean ± SEM). Scale bar is 100 μm. * Results with P values < 0.05 were considered significant. ** Results with P values < 0.01 were considered very significant.

Article Snippet: The cultured cells were randomly divided into three groups according to the experimental design: the control, S100A8 (0.5 μg/mL, HY- P71275 ; MCE, Shanghai, China), and S100A8 + FPS-ZM 1 (5 μM, HY-19370; MCE, Shanghai, China) groups.

Techniques: Control, Immunohistochemical staining, Cell Culture, In Vitro

Journal: Scientific Reports

Article Title: S100A8 regulated by estrogen improves injured endometrial epithelium reconstruction by promoting tight junction formation and stromal cell transformation

doi: 10.1038/s41598-025-08530-0

Figure Lengend Snippet: Effects of S100A8 on tight junctions of endometrial epithelium or endometrial cells. ( a ) Immunohistochemical staining showing Claudin-1 distribution in the endometrium of different groups (control, injury, P407, and P407 + S100A8 groups); black arrows show Claudin-1 accumulated below the cell membrane of the lateral contact zone between adjacent cells and red arrows show cells expressing Claudin-1 in the stroma. Scale bar is 100 μm. ( b ) Claudin-1 expression in the endometrium of different groups (n = 10, mean ± SEM). ( c ) Western blot showing ZO-1 expression in endometrial cells of three different groups (control, S100A8, and S100A8 + FPS-ZM1 groups, n = 3, mean ± SEM). Actin was used as the loading control. The full-length bands can be found in supplementary Fig. 1. The bands of ZO-1 and actin cropped from different parts of the same gel. ( d ) Immunofluorescence showing the co-expression of Claudin-1 (red) and ZO-1 (green) in the endometrial cells of the three groups (n = 5, mean ± SEM). The nucleus is stained blue. The scale bar is 200 μm. * Results with P values < 0.05 were considered significant. ** Results with P values < 0.01 were considered very significant.

Article Snippet: The cultured cells were randomly divided into three groups according to the experimental design: the control, S100A8 (0.5 μg/mL, HY- P71275 ; MCE, Shanghai, China), and S100A8 + FPS-ZM 1 (5 μM, HY-19370; MCE, Shanghai, China) groups.

Techniques: Immunohistochemical staining, Staining, Control, Membrane, Expressing, Western Blot, Immunofluorescence

Journal: Scientific Reports

Article Title: S100A8 regulated by estrogen improves injured endometrial epithelium reconstruction by promoting tight junction formation and stromal cell transformation

doi: 10.1038/s41598-025-08530-0

Figure Lengend Snippet: Effects of S100A8 on endometrial “double-featured” cells. ( a ) Vimentin (red) and ZO-1 (green) immunofluorescent double staining of cultured endometrial cells. Scale bar is 200 μm. ( b ) Western blot showing CK-18 and vimentin expression in endometrial cells from each group (control, S100A8, and FPS-ZM1 groups; n = 3, mean ± SEM). The full-length bands can be found in supplementary Fig. 1. Actin was used as the loading control. As the target proteins have a similar molecular weight to that of the loading control, the bands of CK18/vimentin and actin were cropped from different gels. ( c ) Immunofluorescence showing vimentin expression in endometrial cells of each group (n = 5, mean ± SEM). Scale bar is 200 μm. * Results with P values < 0.05 were considered significant. ** Results with P values < 0.01 were considered very significant.

Article Snippet: The cultured cells were randomly divided into three groups according to the experimental design: the control, S100A8 (0.5 μg/mL, HY- P71275 ; MCE, Shanghai, China), and S100A8 + FPS-ZM 1 (5 μM, HY-19370; MCE, Shanghai, China) groups.

Techniques: Double Staining, Cell Culture, Western Blot, Expressing, Control, Molecular Weight, Immunofluorescence

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Transcriptomics based identification of S100A3 as the key anti-hepatitis B virus factor of 16F16.

doi: 10.1016/j.biopha.2023.114904

Figure Lengend Snippet: Fig. 9. HepG2.2.15 cell line treated with different concentrations of 16F16 drug. (A) Western blot analysis of the expression levels of S100A3 in hepG2.2.15 cells treated with 16F16, which were also consistent with the qPCR analysis, S100A3 is also downregulated at 4 μg/ mL concentration of 16F16 in western blot analysis. Asterisks indicate statistical signifi cance (*P < 0.05, **P < 0.01, ***P < 0.001). (B) qPCR analysis of the transcription of S100A3 in hepG2.2.15 cells treated with 16F16, it was shown that at 4 μg/mL concentration of 16F16 is effective in downregulating S100A3 transcript in HepG2.2.15 cell line. All experi ments were repeated three times.

Article Snippet: The membranes were incubated with the primary S100A3 antibody (sc-514339, 1:1000), PDIA2 antibody (BST19364904, BOSTER Biological Technology), PDIA6 antibody (A03813–2, BOSTER Biological Technology), EREG antibody (ZP3681BP81, BOSTER Biological Technology) and GAPDH (GB12002, 1/1000) overnight at 4◦C.

Techniques: Western Blot, Expressing, Concentration Assay

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Transcriptomics based identification of S100A3 as the key anti-hepatitis B virus factor of 16F16.

doi: 10.1016/j.biopha.2023.114904

Figure Lengend Snippet: Fig. 10. HepG2.2.15 treatment with S100A3-expressing plasmid pLVX-puro-S100A3. (A and B) HepG2.2.15 cell line was treated with pLVX-puro-S100A3, super natant was collected at different time intervals to elucidate effect of S100A3 upregulation on HBsAg and HBeAg, results indicated that S100A3 upregulation results in upregulation of HBsAg and HBeAg. (C) S100A3 also found to be effective in modulating HBV genome, HBV genome was also increased after pLVX-puro-S100A3 treatment in HepG2.2.15 cell line. (D) mRNA expression of S100A3, HBV DNA and HBsAg mRNA in HepG2.2.15 cells expressing the S100A3 gene by pLVX- puro-S100A3, determined using reverse transcription-quantitative polymerase chain reaction analysis. (E) Western blot analysis of HepG2.2.15 cell line after transfection with pLVX-puro-S100A3.

Article Snippet: The membranes were incubated with the primary S100A3 antibody (sc-514339, 1:1000), PDIA2 antibody (BST19364904, BOSTER Biological Technology), PDIA6 antibody (A03813–2, BOSTER Biological Technology), EREG antibody (ZP3681BP81, BOSTER Biological Technology) and GAPDH (GB12002, 1/1000) overnight at 4◦C.

Techniques: Expressing, Plasmid Preparation, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Transfection

Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Article Title: Transcriptomics based identification of S100A3 as the key anti-hepatitis B virus factor of 16F16.

doi: 10.1016/j.biopha.2023.114904

Figure Lengend Snippet: Fig. 11. S100A3 knockdown modulates secretion of HBV antigens and HBV DNA (A-B) S100A3-shRNA is used for knockdown the expression of S100A3, HBsAg and HBeAg were downregulated after treatment with shS100A3. (C) qPCR analysis showed that after S100A3 knock down mRNA levels of HBx and HBs proteins were significantly reduced as compared to control and HepG2.2.15 cells. (D) HBV DNA decreased after shS100A3 treatment in time dependent manner as compared to control and HepG2.2.15 cells, determined by using reverse transcription-quantitative polymerase chain reaction analysis. (E) Western blot analysis verified the successful knockdown of S100A3 in HepG2.2.15 cell line.

Article Snippet: The membranes were incubated with the primary S100A3 antibody (sc-514339, 1:1000), PDIA2 antibody (BST19364904, BOSTER Biological Technology), PDIA6 antibody (A03813–2, BOSTER Biological Technology), EREG antibody (ZP3681BP81, BOSTER Biological Technology) and GAPDH (GB12002, 1/1000) overnight at 4◦C.

Techniques: Knockdown, shRNA, Expressing, Control, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot