Review

leptin rabbit anti human polyclonal antibody (Cusabio)

Cusabio is a verified supplier

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Cusabio leptin rabbit anti human polyclonal antibody

Figure 1. Immunohistochemical staining of <t>Leptin,</t> OPG, and RANKL in control and chronic periodontitis groups. A-C. Immunohistochemical staining of Leptin in the control group(A), the moderate chronic periodontitis group (B), and the severe chronic periodontitis group (C). D-F. Immunohistochemical staining of OPG in the control group (D), the moderate chronic periodontitis group (E), and the severe chronic periodontitis group (F). G-I. Immunohistochemical staining of RANKL in the control group (G), the moderate chronic periodontitis group (H), and the severe chronic periodontitis group (I). Red arrows indicate the positive cells. EL: epithelial layer, LP: lamina propria.

Leptin Rabbit Anti Human Polyclonal Antibody, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/leptin+rabbit+anti+human+polyclonal+antibody/pm33967621-64-0-6?v=Cusabio
Average 93 stars, based on 1 article reviews

leptin rabbit anti human polyclonal antibody - by Bioz Stars, 2026-07

93/100 stars

Images

1) Product Images from "Leptin regulates OPG and RANKL expression in Gingival Fibroblasts and Tissues of Chronic Periodontitis Patients."

Article Title: Leptin regulates OPG and RANKL expression in Gingival Fibroblasts and Tissues of Chronic Periodontitis Patients.

Journal: International journal of medical sciences

doi: 10.7150/ijms.56151

Figure 1. Immunohistochemical staining of Leptin, OPG, and RANKL in control and chronic periodontitis groups. A-C. Immunohistochemical staining of Leptin in the control group(A), the moderate chronic periodontitis group (B), and the severe chronic periodontitis group (C). D-F. Immunohistochemical staining of OPG in the control group (D), the moderate chronic periodontitis group (E), and the severe chronic periodontitis group (F). G-I. Immunohistochemical staining of RANKL in the control group (G), the moderate chronic periodontitis group (H), and the severe chronic periodontitis group (I). Red arrows indicate the positive cells. EL: epithelial layer, LP: lamina propria.

Figure Legend Snippet: Figure 1. Immunohistochemical staining of Leptin, OPG, and RANKL in control and chronic periodontitis groups. A-C. Immunohistochemical staining of Leptin in the control group(A), the moderate chronic periodontitis group (B), and the severe chronic periodontitis group (C). D-F. Immunohistochemical staining of OPG in the control group (D), the moderate chronic periodontitis group (E), and the severe chronic periodontitis group (F). G-I. Immunohistochemical staining of RANKL in the control group (G), the moderate chronic periodontitis group (H), and the severe chronic periodontitis group (I). Red arrows indicate the positive cells. EL: epithelial layer, LP: lamina propria.

Techniques Used: Immunohistochemical staining, Staining, Control

Figure 2. RANKL and OPG expression levels in leptin-treated HGF. A. Immunohistochemical staining of vimentin in HGF. B. Immunohistochemical staining of keratin in HGF. C. Expression of OPG, RANKL and OPG/RANKL at mRNA level in different leptin concentration groups (ug/ml).

Figure Legend Snippet: Figure 2. RANKL and OPG expression levels in leptin-treated HGF. A. Immunohistochemical staining of vimentin in HGF. B. Immunohistochemical staining of keratin in HGF. C. Expression of OPG, RANKL and OPG/RANKL at mRNA level in different leptin concentration groups (ug/ml).

Techniques Used: Expressing, Immunohistochemical staining, Staining, Concentration Assay

Image Search Results

Journal: International journal of medical sciences

Article Title: Leptin regulates OPG and RANKL expression in Gingival Fibroblasts and Tissues of Chronic Periodontitis Patients.

doi: 10.7150/ijms.56151

Figure Lengend Snippet: Figure 1. Immunohistochemical staining of Leptin, OPG, and RANKL in control and chronic periodontitis groups. A-C. Immunohistochemical staining of Leptin in the control group(A), the moderate chronic periodontitis group (B), and the severe chronic periodontitis group (C). D-F. Immunohistochemical staining of OPG in the control group (D), the moderate chronic periodontitis group (E), and the severe chronic periodontitis group (F). G-I. Immunohistochemical staining of RANKL in the control group (G), the moderate chronic periodontitis group (H), and the severe chronic periodontitis group (I). Red arrows indicate the positive cells. EL: epithelial layer, LP: lamina propria.

Article Snippet: Leptin Rabbit Anti-Human Polyclonal Antibody (CSB-PA009805, CUSABIO, China), OPG Rabbit AntiHuman Polyclonal Antibody (CSB-PA003597, CUSABIO, China), RANKL Rabbit Anti-Human Polyclonal Antibody (CSB-PA023986LA01HU, CUSABIO, China), DAB (Servicebio, China), Dulbecco’s Modified Eagle Medium (DMEM), Fetal Bovine Serum (Hyclone, America), Trypsin (Gibco, America), TRizol, PrimeScript RT reagent kit, SYBR Green mix (CWBIO, China) were used.

Techniques: Immunohistochemical staining, Staining, Control

Journal: International journal of medical sciences

Article Title: Leptin regulates OPG and RANKL expression in Gingival Fibroblasts and Tissues of Chronic Periodontitis Patients.

doi: 10.7150/ijms.56151

Figure Lengend Snippet: Figure 2. RANKL and OPG expression levels in leptin-treated HGF. A. Immunohistochemical staining of vimentin in HGF. B. Immunohistochemical staining of keratin in HGF. C. Expression of OPG, RANKL and OPG/RANKL at mRNA level in different leptin concentration groups (ug/ml).

Techniques: Expressing, Immunohistochemical staining, Staining, Concentration Assay

Figure 1 Inhibition of NFκB suppressed E2 effect on leptin expression BeWo cells (A) and (C) and term placental explants (B) and (D) were pretreated as indicated with sulfasalazine during 30 min, afterwards E2 was added. After 48 h (A) or 24 h (B), total RNA was extracted and Leptin mRNA expression was quantified by qRT-PCR. Cyclophilin was used as internal standard. Cell extracts (C) and placental explants extracts (D) were prepared as indicated in ‘Materials and methods’ section and proteins were separated on 12% SDS-PAGE gel. Leptin expression was determined by Western blot. Loading control was performed by immunoblotting the same membranes with anti-GAPDH. Standard protein markers were used to estimate the molecular weights. Molecular weight (kDa) is indicated at the right of each blot. Bands densitometry is shown in lower panels. Results are expressed as mean ± s.d. for ten independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 vs control and ##P < 0.01, ###P < 0.001 vs E2 treatment. Statistical analyses were performed by ANOVA followed by Bonferroni post hoc test.

Journal: Reproduction

Article Title: Crosstalk between estradiol and NFκB signaling pathways on placental leptin expression

doi: 10.1530/rep-20-0142

Figure Lengend Snippet: Figure 1 Inhibition of NFκB suppressed E2 effect on leptin expression BeWo cells (A) and (C) and term placental explants (B) and (D) were pretreated as indicated with sulfasalazine during 30 min, afterwards E2 was added. After 48 h (A) or 24 h (B), total RNA was extracted and Leptin mRNA expression was quantified by qRT-PCR. Cyclophilin was used as internal standard. Cell extracts (C) and placental explants extracts (D) were prepared as indicated in ‘Materials and methods’ section and proteins were separated on 12% SDS-PAGE gel. Leptin expression was determined by Western blot. Loading control was performed by immunoblotting the same membranes with anti-GAPDH. Standard protein markers were used to estimate the molecular weights. Molecular weight (kDa) is indicated at the right of each blot. Bands densitometry is shown in lower panels. Results are expressed as mean ± s.d. for ten independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001 vs control and ##P < 0.01, ###P < 0.001 vs E2 treatment. Statistical analyses were performed by ANOVA followed by Bonferroni post hoc test.

Article Snippet: Membranes were equilibrated in 1× PBS and non-specific binding sites were blocked with 5% non-fat milk in PBS at room temperature for 1 h. Then they were immunoblotted with the specific polyclonal rabbit anti-human leptin Y20 (1:1000, Santa Cruz Biotechnology, Inc.), monoclonal mouse anti-p65 (1:1000, Santa Cruz Biotechnology, Inc.), or monoclonal mouse anti-pIκBα (1:1000 Santa Cruz Biotechnology, Inc.).

Techniques: Inhibition, Expressing, Quantitative RT-PCR, SDS Page, Western Blot, Control, Molecular Weight

Figure 2 Effect of p65 overexpression on E2 induced placental leptin expression. (A) BeWo cells were transiently transfected with pL1951 plasmid construction containing the promoter region of leptin gene from −1951 to +42 bp and different amounts of p65 expression plasmid. After transfection, BeWo cells were incubated for 48 h in DMEM-F12 media supplemented with 1% FBS and treated with E2 as indicated. (B) BeWo cells were transiently transfected with pL1951 plasmid construction, different amounts of plasmid expressing human

Journal: Reproduction

Article Title: Crosstalk between estradiol and NFκB signaling pathways on placental leptin expression

doi: 10.1530/rep-20-0142

Figure Lengend Snippet: Figure 2 Effect of p65 overexpression on E2 induced placental leptin expression. (A) BeWo cells were transiently transfected with pL1951 plasmid construction containing the promoter region of leptin gene from −1951 to +42 bp and different amounts of p65 expression plasmid. After transfection, BeWo cells were incubated for 48 h in DMEM-F12 media supplemented with 1% FBS and treated with E2 as indicated. (B) BeWo cells were transiently transfected with pL1951 plasmid construction, different amounts of plasmid expressing human

Techniques: Over Expression, Expressing, Transfection, Plasmid Preparation, Incubation

Figure 1. Analysis of surgical ATAA samples collected from patients with a variety of diseases underlying ATAA. A through C, Hypertension and hypercholesterolemia. D through F, Marfan syndrome. G through I, Ankylosing spondylitis. A, D, and G, Diffuse elastic ﬁber fragmentation with glycosaminoglycan deposition (bluish-green), matrix clearing, and media degeneration, Movat’s pentachrome. Scale bar=250 lm. B, E, and H, Leptin immunostaining in medial smooth muscle cells. Scale bar=50 lm. C, F, I, and L, The lep mRNA (black staining) is present in diseased aortas but is scarcely present in normal aorta. Scale bar=10 lm. J and K, Positive (antisense) (J) and negative (sense) (K) control for lep mRNA. In situ hybridization in human WAT. Scale bar=10 lm. ATAA indicates ascending thoracic aortic aneurysm; IHC, immunohistochemistry; WAT, white adipose tissue.

Journal: Journal of the American Heart Association

Article Title: Local Application of Leptin Antagonist Attenuates Angiotensin II–Induced Ascending Aortic Aneurysm and Cardiac Remodeling

doi: 10.1161/jaha.116.003474

Figure Lengend Snippet: Figure 1. Analysis of surgical ATAA samples collected from patients with a variety of diseases underlying ATAA. A through C, Hypertension and hypercholesterolemia. D through F, Marfan syndrome. G through I, Ankylosing spondylitis. A, D, and G, Diffuse elastic ﬁber fragmentation with glycosaminoglycan deposition (bluish-green), matrix clearing, and media degeneration, Movat’s pentachrome. Scale bar=250 lm. B, E, and H, Leptin immunostaining in medial smooth muscle cells. Scale bar=50 lm. C, F, I, and L, The lep mRNA (black staining) is present in diseased aortas but is scarcely present in normal aorta. Scale bar=10 lm. J and K, Positive (antisense) (J) and negative (sense) (K) control for lep mRNA. In situ hybridization in human WAT. Scale bar=10 lm. ATAA indicates ascending thoracic aortic aneurysm; IHC, immunohistochemistry; WAT, white adipose tissue.

Article Snippet: For identification of leptin and its specific receptor (LepR), paraffin cross-sections were incubated overnight at 4°C with a rabbit polyclonal antibody against human leptin or human LepR (1:200 or 1:100, respectively; Santa Cruz Biotechnology Inc.).

Techniques: Immunostaining, Staining, Control, In Situ Hybridization, Immunohistochemistry

Figure 2. The effects of locally applied leptin on the ascending aorta. A, Human arch arteriogram depicting mouse aortic anatomy. Note the location of leptin slow-release ﬁlm (yellow) in relation to the aortic valve level (white dashed lines). B, Increase in maximal aortic diameter from baseline following treatment with leptin in diastole and systole (P=0.02 and P=0.045, respectively). Baseline aortic diameter was 1.3 mm. C, Percentage of aortic wall distensibility assessed at baseline and 4 weeks after surgery (P=0.01; n=10 to 11). Control mice in white bars, leptin treated in gray bars. *P<0.05. D through G, Histologic cross-sections of the ascending aortic at the location of leptin application, as shown in (A). Elastic Van Gieson (EVG) staining shows fragmentations of elastic lamellae (arrows) in leptin treated (D) and control mice (E). Depletion of a-smooth muscle actin (a-SMA) immunostaining (arrow) in leptin treated (F) and control mice (G). Scale bar=100 lm, 200 lm for (D0 and E0).

Journal: Journal of the American Heart Association

Article Title: Local Application of Leptin Antagonist Attenuates Angiotensin II–Induced Ascending Aortic Aneurysm and Cardiac Remodeling

doi: 10.1161/jaha.116.003474

Figure Lengend Snippet: Figure 2. The effects of locally applied leptin on the ascending aorta. A, Human arch arteriogram depicting mouse aortic anatomy. Note the location of leptin slow-release ﬁlm (yellow) in relation to the aortic valve level (white dashed lines). B, Increase in maximal aortic diameter from baseline following treatment with leptin in diastole and systole (P=0.02 and P=0.045, respectively). Baseline aortic diameter was 1.3 mm. C, Percentage of aortic wall distensibility assessed at baseline and 4 weeks after surgery (P=0.01; n=10 to 11). Control mice in white bars, leptin treated in gray bars. *P<0.05. D through G, Histologic cross-sections of the ascending aortic at the location of leptin application, as shown in (A). Elastic Van Gieson (EVG) staining shows fragmentations of elastic lamellae (arrows) in leptin treated (D) and control mice (E). Depletion of a-smooth muscle actin (a-SMA) immunostaining (arrow) in leptin treated (F) and control mice (G). Scale bar=100 lm, 200 lm for (D0 and E0).

Techniques: Control, Staining, Immunostaining

$Figure 3. Leptin applied at the ascending aorta induces remodeling of LV wall and valve leaﬂets. A, Leptin-induced increase in PSV measured at the aortic valve. P=0.17. Mean baseline PSV was 1150 mm/s. B, Leptin induced an increase in LV wall thickness, as measured in the long-axis view (P=0.06), and in diastole, as measured in the short-axis view (P=0.045). Mean LV wall thickness at baseline was 0.83 mm at anterior and posterior walls and 0.55 mm at the septum. C, Increase in LV diameter following treatment with leptin in diastole (P=0.11) and in systole (P=0.04). Mean LV diameter at baseline was 2.2 mm. D, Difference in FAC following treatment with leptin (P=0.09). Mean FAC at baseline was 63%. E, Thickness of mitral and aortic valve leaﬂets following leptin treatment (P=0.02 and P=0.006, respectively). A through E, n=9 to 11. Control mice shown in white bars; leptin-treated mice shown in dark gray bars. F and G, H&E staining of mitral valve from leptin-treated (F) and control (G) mice. Arrows point to the valve. Scale bar=100 lm. H and I, H&E staining of aortic valve from leptin-treated (H) and control (I) mice. Arrows point to the valve. J and K, a-SMA staining in aortic valves of leptin-treated mice (J) and controls (K). L and M, TGF-b1 expression in aortic valves of leptin-treated mice (L) and controls (M). Scale bar: Low magniﬁcation=50 lm, enlargements=100 lm. *P<0.05, **P<0.01. a-SMA indicates a- smooth muscle cell actin; FAC, fractional area change; H&E, hematoxylin and eosin; LV, left ventricular; PSV, peak systolic velocity; TGF-b1, transforming growth factor b1.$

Journal: Journal of the American Heart Association

Article Title: Local Application of Leptin Antagonist Attenuates Angiotensin II–Induced Ascending Aortic Aneurysm and Cardiac Remodeling

doi: 10.1161/jaha.116.003474

Figure Lengend Snippet: Figure 3. Leptin applied at the ascending aorta induces remodeling of LV wall and valve leaﬂets. A, Leptin-induced increase in PSV measured at the aortic valve. P=0.17. Mean baseline PSV was 1150 mm/s. B, Leptin induced an increase in LV wall thickness, as measured in the long-axis view (P=0.06), and in diastole, as measured in the short-axis view (P=0.045). Mean LV wall thickness at baseline was 0.83 mm at anterior and posterior walls and 0.55 mm at the septum. C, Increase in LV diameter following treatment with leptin in diastole (P=0.11) and in systole (P=0.04). Mean LV diameter at baseline was 2.2 mm. D, Difference in FAC following treatment with leptin (P=0.09). Mean FAC at baseline was 63%. E, Thickness of mitral and aortic valve leaﬂets following leptin treatment (P=0.02 and P=0.006, respectively). A through E, n=9 to 11. Control mice shown in white bars; leptin-treated mice shown in dark gray bars. F and G, H&E staining of mitral valve from leptin-treated (F) and control (G) mice. Arrows point to the valve. Scale bar=100 lm. H and I, H&E staining of aortic valve from leptin-treated (H) and control (I) mice. Arrows point to the valve. J and K, a-SMA staining in aortic valves of leptin-treated mice (J) and controls (K). L and M, TGF-b1 expression in aortic valves of leptin-treated mice (L) and controls (M). Scale bar: Low magniﬁcation=50 lm, enlargements=100 lm. *P<0.05, **P<0.01. a-SMA indicates a- smooth muscle cell actin; FAC, fractional area change; H&E, hematoxylin and eosin; LV, left ventricular; PSV, peak systolic velocity; TGF-b1, transforming growth factor b1.

Techniques: Control, Staining, Expressing

Figure 4. Local application of LepA at the proximal ascending aorta attenuates the effects of AngII infusion on the aortic wall locally. A and B, External aortic diameter 4 weeks after surgery. n=5, P=0.047. C, Increase in aorta diameter in diastole and systole (P<0.01 in systole). Mean internal aortic diameter was 1.3 mm at baseline. D, Aortic distensibility at baseline and 4 weeks after surgery. C and D, n=12 to 13. E, AngII infusion leads to fatal rupture of TAA or AAA. Surviving mice were euthanized 4 weeks after surgery. Application of LepA abolished TAA rupture (P=0.01, 2-tailed Fisher exact test). F, A Kaplan–Meier survival curve for mice receiving AngII infusion or AngII cotreated with LepA. G, Leptin was detected in smooth muscle cells (open arrowheads) and atherosclerotic plaques (black arrowhead) but was barely detected in control mice treated with an empty polylactic co–glycolic acid ﬁlm. Scale bar=50 lm. H and I, Macrophage inﬁltration in AngII (H) and AngII and LepA-treated mice (I). Open arrowhead points to inﬁltrating macrophages, black arrowheads point to macrophages in the adventitia. Scale bar=50 lm. We did not detect macrophages inﬁltrating the media of LepA-treated mice (I). J, Number of breaks in aortic elastic lamellas. P=0.05, n=5 to 6. K and L0, Ascending aorta from AngII (K) and AngII and LepA-treated mice (L) stained by EVG; black arrowheads highlight fragmentation of elastic lamellae. Scale bar=100 lm. M and N0, Immunostaining of a-SMA in similar location as (K and L0); black arrowhead highlights an absence of a- SMA. Scale bar=100 lm. *P<0.05, **P<0.01. a-SMA indicates a-smooth muscle cell actin; AAA, abdominal aortic aneurysm; AngII, angiotensin II; EVG, elastic Van Gieson; LepA, leptin antagonist; TAA, thoracic aortic aneurysm.

Journal: Journal of the American Heart Association

Article Title: Local Application of Leptin Antagonist Attenuates Angiotensin II–Induced Ascending Aortic Aneurysm and Cardiac Remodeling

doi: 10.1161/jaha.116.003474

Figure Lengend Snippet: Figure 4. Local application of LepA at the proximal ascending aorta attenuates the effects of AngII infusion on the aortic wall locally. A and B, External aortic diameter 4 weeks after surgery. n=5, P=0.047. C, Increase in aorta diameter in diastole and systole (P<0.01 in systole). Mean internal aortic diameter was 1.3 mm at baseline. D, Aortic distensibility at baseline and 4 weeks after surgery. C and D, n=12 to 13. E, AngII infusion leads to fatal rupture of TAA or AAA. Surviving mice were euthanized 4 weeks after surgery. Application of LepA abolished TAA rupture (P=0.01, 2-tailed Fisher exact test). F, A Kaplan–Meier survival curve for mice receiving AngII infusion or AngII cotreated with LepA. G, Leptin was detected in smooth muscle cells (open arrowheads) and atherosclerotic plaques (black arrowhead) but was barely detected in control mice treated with an empty polylactic co–glycolic acid ﬁlm. Scale bar=50 lm. H and I, Macrophage inﬁltration in AngII (H) and AngII and LepA-treated mice (I). Open arrowhead points to inﬁltrating macrophages, black arrowheads point to macrophages in the adventitia. Scale bar=50 lm. We did not detect macrophages inﬁltrating the media of LepA-treated mice (I). J, Number of breaks in aortic elastic lamellas. P=0.05, n=5 to 6. K and L0, Ascending aorta from AngII (K) and AngII and LepA-treated mice (L) stained by EVG; black arrowheads highlight fragmentation of elastic lamellae. Scale bar=100 lm. M and N0, Immunostaining of a-SMA in similar location as (K and L0); black arrowhead highlights an absence of a- SMA. Scale bar=100 lm. *P<0.05, **P<0.01. a-SMA indicates a-smooth muscle cell actin; AAA, abdominal aortic aneurysm; AngII, angiotensin II; EVG, elastic Van Gieson; LepA, leptin antagonist; TAA, thoracic aortic aneurysm.

Techniques: Control, Staining, Immunostaining

$Figure 5. Local application of LepA at the proximal ascending aorta attenuates the effects of AngII infusion on LV remodeling. A, Increase in PSV measured at the aortic valve. P=0.03. AngII-infused mice shown in white bars; AngII and LepA shown in dark gray bars. Mean PSV at baseline was 1275 mm/s. B, Increase in LV wall thickness as measured by echocardiography in long axis (P<0.01) and in diastole in short axis views (P<0.01). Mean LV wall thickness at baseline was 0.79 mm at anterior and posterior walls and 0.57 mm at the septum. C, Increase in LV diameter in diastole (P=0.047) and systole. Mean LV diameter was 2.3 mm at baseline. D, FAC is reduced in AngII-infused mice but is not affected in AngII and LepA-treated mice. P=0.01. Mean FAC was 55% at baseline. E, Mitral and aortic valve leaﬂets thickness is reduced in AngII and LepA-treated mice compared with AngII-infused mice. P=0.03 for both valves. A through E, n=10 to 12. F and G, H&E staining of a mitral valve from AngII (F) and AngII and LepA-treated mice (G). Arrows point to the valve. H and I, H&E staining of an aortic valve from AngII (H) and AngII and LepA-treated mice (I). Arrows point to the valve. J and K, a-SMA is abundant in aortic valves of AngII-infused mice (J), with relatively weaker expression in AngII and LepA-treated mice (K). L and M, TGF-b1 expression is widespread in aortic valves of AngII-infused mice (L) but is less prevalent in AngII and LepA-treated mice (M). Scale bar=100 lm (F through M). *P<0.05, **P<0.01. a-SMA indicates a-smooth muscle cell actin; AngII, angiotensin II; FAC, fractional area change; H&E, hematoxylin and eosin; LepA, leptin antagonist; LV, left ventricular; PSV, peak systolic velocity; TGF-b1, transforming growth factor b1.$

Journal: Journal of the American Heart Association

Article Title: Local Application of Leptin Antagonist Attenuates Angiotensin II–Induced Ascending Aortic Aneurysm and Cardiac Remodeling

doi: 10.1161/jaha.116.003474

Figure Lengend Snippet: Figure 5. Local application of LepA at the proximal ascending aorta attenuates the effects of AngII infusion on LV remodeling. A, Increase in PSV measured at the aortic valve. P=0.03. AngII-infused mice shown in white bars; AngII and LepA shown in dark gray bars. Mean PSV at baseline was 1275 mm/s. B, Increase in LV wall thickness as measured by echocardiography in long axis (P<0.01) and in diastole in short axis views (P<0.01). Mean LV wall thickness at baseline was 0.79 mm at anterior and posterior walls and 0.57 mm at the septum. C, Increase in LV diameter in diastole (P=0.047) and systole. Mean LV diameter was 2.3 mm at baseline. D, FAC is reduced in AngII-infused mice but is not affected in AngII and LepA-treated mice. P=0.01. Mean FAC was 55% at baseline. E, Mitral and aortic valve leaﬂets thickness is reduced in AngII and LepA-treated mice compared with AngII-infused mice. P=0.03 for both valves. A through E, n=10 to 12. F and G, H&E staining of a mitral valve from AngII (F) and AngII and LepA-treated mice (G). Arrows point to the valve. H and I, H&E staining of an aortic valve from AngII (H) and AngII and LepA-treated mice (I). Arrows point to the valve. J and K, a-SMA is abundant in aortic valves of AngII-infused mice (J), with relatively weaker expression in AngII and LepA-treated mice (K). L and M, TGF-b1 expression is widespread in aortic valves of AngII-infused mice (L) but is less prevalent in AngII and LepA-treated mice (M). Scale bar=100 lm (F through M). *P<0.05, **P<0.01. a-SMA indicates a-smooth muscle cell actin; AngII, angiotensin II; FAC, fractional area change; H&E, hematoxylin and eosin; LepA, leptin antagonist; LV, left ventricular; PSV, peak systolic velocity; TGF-b1, transforming growth factor b1.

Techniques: Staining, Expressing

Figure 6. Leptin is expressed in AVs of AVS patients and induces VIC proliferation and calciﬁcation in vitro. A, Movat staining of healthy human AV. Arrowhead points to ascending aorta, arrow to AV. B and C, Movat (B) and leptin IHC (C) of AV collected from an AVS patient. D and E, LepR (D) and leptin (E) IHC from the same valve as in (B and C). Arrows point to macrophage-like cells; arrowheads point to elongated SMC smooth muscle-like cells. F, qPCR analysis for lep and lepr expression in AVs. n=3 and n=8 for valves of healthy and AVS patients, respectively. G, Positive correlation between lep and lepr expression in AVs. r2=0.76 (Spearman correlation), P=0.007. H through K, In vitro primary human VICs. H, AngII increases VIC proliferation. This effect is blocked by the AngII type 1 receptor blocker valsartan and LepA. (P=0.01; n=5–6). I, qPCR analysis for lepr and lep expression in VICs treated with AngII for 4 or 24 hours compared with untreated VICs. P=0.046, P=0.007 (4 hours), P<0.001 (24 hours). Error bars represent standard deviation. J, Leptin increases VICs proliferation (P=0.01), and this effect is blocked by LepA (P=0.01; n=6). K, Mineralization of VICs grown in osteogenic medium is increased by leptin (P<0.05; n=3). *P<0.05, **P<0.01. AngII indicates angiotensin II; AV, aortic valve; AVS, aortic valve stenosis; IHC, immunohistochemistry; LepA, leptin antagonist; LepR, leptin receptor; qPCR, quantitative polymerase chain reaction; Val, valsartan; VIC, valve interstitial cell.

Journal: Journal of the American Heart Association

Article Title: Local Application of Leptin Antagonist Attenuates Angiotensin II–Induced Ascending Aortic Aneurysm and Cardiac Remodeling

doi: 10.1161/jaha.116.003474

Figure Lengend Snippet: Figure 6. Leptin is expressed in AVs of AVS patients and induces VIC proliferation and calciﬁcation in vitro. A, Movat staining of healthy human AV. Arrowhead points to ascending aorta, arrow to AV. B and C, Movat (B) and leptin IHC (C) of AV collected from an AVS patient. D and E, LepR (D) and leptin (E) IHC from the same valve as in (B and C). Arrows point to macrophage-like cells; arrowheads point to elongated SMC smooth muscle-like cells. F, qPCR analysis for lep and lepr expression in AVs. n=3 and n=8 for valves of healthy and AVS patients, respectively. G, Positive correlation between lep and lepr expression in AVs. r2=0.76 (Spearman correlation), P=0.007. H through K, In vitro primary human VICs. H, AngII increases VIC proliferation. This effect is blocked by the AngII type 1 receptor blocker valsartan and LepA. (P=0.01; n=5–6). I, qPCR analysis for lepr and lep expression in VICs treated with AngII for 4 or 24 hours compared with untreated VICs. P=0.046, P=0.007 (4 hours), P<0.001 (24 hours). Error bars represent standard deviation. J, Leptin increases VICs proliferation (P=0.01), and this effect is blocked by LepA (P=0.01; n=6). K, Mineralization of VICs grown in osteogenic medium is increased by leptin (P<0.05; n=3). *P<0.05, **P<0.01. AngII indicates angiotensin II; AV, aortic valve; AVS, aortic valve stenosis; IHC, immunohistochemistry; LepA, leptin antagonist; LepR, leptin receptor; qPCR, quantitative polymerase chain reaction; Val, valsartan; VIC, valve interstitial cell.

Techniques: In Vitro, Staining, Expressing, Standard Deviation, Immunohistochemistry, Real-time Polymerase Chain Reaction

Review

Structured Review

Images

1) Product Images from "Leptin regulates OPG and RANKL expression in Gingival Fibroblasts and Tissues of Chronic Periodontitis Patients."

Similar Products

Image Search Results