Journal: bioRxiv

Article Title: A novel mouse model of hypertensive emergency with multiorgan microvascular disease implicating the VEGFA/sFlt-1 balance

doi: 10.64898/2026.03.03.709451

Figure Lengend Snippet: A- Mice survival after hypertension onset (days after beginning of Ang II infusion). N= 20 C57BL6/J (B6J) and 129Sv (129) B- Mean daytime telemetry blood pressure N= 4 B6J and 129Sv. Values represent mean ± SEM. C- Mean nighttime telemetry blood pressure. N= 4 B6J and 129Sv. Values represent mean ± SEM.

Article Snippet: The hypertensive model was induced by subcutaneous infusion of angiotensin II (Ang II) (Alomone, GPA-100) at 1 μg/kg/min for 7 or 14 days, via osmotic minipumps (Alzet, model 1007D or 1002) in 10- to 16-week-old males.

Techniques:

Journal: bioRxiv

Article Title: A novel mouse model of hypertensive emergency with multiorgan microvascular disease implicating the VEGFA/sFlt-1 balance

doi: 10.64898/2026.03.03.709451

Figure Lengend Snippet: A- In vivo imaging (microm) performed on 129Sv (129) and C57BL6/J (B6J) mice 8 days after angiotensin-2 pump implantation shows haemorrhage (arrows) and hard exudates (asterisks). Haemorrhagic spots are only found on the 129Sv eye fundus and density of hard exudates is increased in 129 mice compared to B6J mice. B-Haemorrhagic spots (arrow heads) in retinas at day 7 of hypertensive challenge and associated quantification. Values represent mean ± SEM of 5 mice per group. * p < 0.05. C- Subretinal swelling assessed by OCT at day 7 of hypertensive challenge and associated quantification. The white arrow shows retinal detachment. D- Retinal capillary density assessed at day 7 of hypertensive challenge. Representative images of the retina vascular network stained with lectin antibody. Values represent mean ± SEM of 4 B6J mice and 8 129 mice. *** p < 0.001.

Article Snippet: The hypertensive model was induced by subcutaneous infusion of angiotensin II (Ang II) (Alomone, GPA-100) at 1 μg/kg/min for 7 or 14 days, via osmotic minipumps (Alzet, model 1007D or 1002) in 10- to 16-week-old males.

Techniques: In Vivo Imaging, Staining

Journal: bioRxiv

Article Title: A novel mouse model of hypertensive emergency with multiorgan microvascular disease implicating the VEGFA/sFlt-1 balance

doi: 10.64898/2026.03.03.709451

Figure Lengend Snippet: Typical ECG changes seen in SV129 mice treated for 2 weeks with angiotensin II (n = 5-7 mice/group. A. episode of atrial flutter B. atrial fibrillation. C. ventricular ectopy seen in the Ang II group; D. short run of ventricular tachycardia; E. sustained ventricular tachycardia degenerating in ventricular fibrillation and cardiac death.

Article Snippet: The hypertensive model was induced by subcutaneous infusion of angiotensin II (Ang II) (Alomone, GPA-100) at 1 μg/kg/min for 7 or 14 days, via osmotic minipumps (Alzet, model 1007D or 1002) in 10- to 16-week-old males.

Techniques:

Journal: Experimental and Therapeutic Medicine

Article Title: Ginsenoside Rg3 induces ginsenoside Rb1-comparable cardioprotective effects independent of reducing blood pressure in spontaneously hypertensive rats

doi: 10.3892/etm.2017.5198

Figure Lengend Snippet: Effects of Rb1 and Rg3 on blood pressure, CWI and RAS activity in the serum. (A) SBP, (B) DBP and (C) PP of rats prior to and following 6 weeks treatment. (D) Body and (E) heart weights and (F) CWI. Serum (G) ACE and (H) Ang II levels. Data are presented as the mean ± standard deviation, n=8 (A-F) or n=6 (G-H) for each group. *P<0.05 vs. WKY group prior to treatment; # P<0.05 vs. WKY group following treatment; $ P<0.05 vs. SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; CWI, cardiac weight index; RAS, renin angiotensin system; SBP, systolic blood pressure; DBP, diastolic blood pressure; PP, pulse pressure; ACE, angiotensin converting enzyme; Ang II, angiotensin II; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.

Article Snippet: ACE (CSB-E04490r) and Ang II (CSB-E04494r) ELISA kits were purchased from Cusabio Biotech Co., Ltd. (Wuhan, China) and the assays were completed by this company.

Techniques: Activity Assay, Standard Deviation

Journal: Experimental and Therapeutic Medicine

Article Title: Ginsenoside Rg3 induces ginsenoside Rb1-comparable cardioprotective effects independent of reducing blood pressure in spontaneously hypertensive rats

doi: 10.3892/etm.2017.5198

Figure Lengend Snippet: Effects of Rb1 and Rg3 on RAS and TGF-β1 levels in the myocardium. (A) Representative IHC staining photomicrographs of myocardium tissue. (Magnification, ×400). Antibodies against ACE, Ang II, AT1 and TGF-β1 were used as the primary antibodies. (B-E) Quantitative results of IHC staining, which were presented as IOD/Area and were proportional to the levels of ACE, Ang II, AT1 and TGF-β1. Data are presented as the mean ± standard deviation, n=4. # P<0.05 vs. the WKY group following treatment; $ P<0.05 vs. the SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; RAS, renin angiotensin system; TGF-β1, transforming growth factor β1; IHC, immunohistochemistry; ACE, angiotensin converting enzyme; Ang II, angiotensin II; AT1, Ang II receptor type 1; IOD, integrated optical density; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.

Article Snippet: ACE (CSB-E04490r) and Ang II (CSB-E04494r) ELISA kits were purchased from Cusabio Biotech Co., Ltd. (Wuhan, China) and the assays were completed by this company.

Techniques: Immunohistochemistry, Standard Deviation

Journal: Acta Biochimica et Biophysica Sinica

Article Title: Activation of angiogenin expression in macrophages by lipopolysaccharide via the TLR4/NF-κB pathway in colitis

doi: 10.3724/abbs.2024013

Figure Lengend Snippet: Table 1 Sequences of primers and siRNAs used in this study

Article Snippet: The membrane was blocked with 5% nonfat milk and then incubated with primary antibodies, including anti-ANG antibody (prepared in our own laboratory) and anti-ACTB antibody (#81115-1-RR; Proteintech, Chicago, USA), in TBST (Tris-buffered saline, 0.1% Tween 20) buffer at 4°C overnight.

Techniques: Negative Control

Journal: American Journal of Translational Research

Article Title: Renal and cerebral RAS interaction contributes to diabetic kidney disease

doi:

Figure Lengend Snippet: Renal RAS, oxidative stress, inflammation and glomerulosclerosis were up-regulated in DM rats. A. Representative photographs and semiquantitative data of AGT, AT1 and MCP-1 expression detected by immunohistochemistry (a1) and Western blot (a2). B. Glomerulosclerosis index measured by PAS. C. Protein level of Noxs in renal cortex measured by Western blot. Data are expressed as the mean ± SD (n=15 in each group). *P<0.05 versus non-DM rats. PAS, periodic acid-Schiff.

Article Snippet: RAS activity in brain Cerebral localization of AGT and AT1 receptors was determined by double-staining immunofluorescence using anti-AGT or anti-AT1 receptors as the first primary antibody, and anti-neuron-specific enolase (Boster Biological Technology, Pleasanton, CA, USA) or anti-glial fibrillary acidic protein (Boster Biological Technology, Pleasanton, CA, USA) as the second primary antibody.

Techniques: Expressing, Immunohistochemistry, Western Blot

Journal: American Journal of Translational Research

Article Title: Renal and cerebral RAS interaction contributes to diabetic kidney disease

doi:

Figure Lengend Snippet: Brain RAS, oxidative stress and sympathetic activity were up-regulated in DM rats. A. AGT and AT1 receptors in SFO (a1), SON (a2) and PVN (a3) measured by immunohistochemistry. B. AGT and AT1 receptors in SFO (b1), SON (b2) and PVN (b3) measured by Western blot. C. Protein levels of NOX2 and NOX4 in SFO (c1), SON (c2) and PVN (c3) measured by Western-blot. D. Representative photographs of TH+c-fos positive cells in RVLM measured by immunohistochemistry. E. Protein levels of TH in RVLM measured by Western-blot. F. Protein levels of TH in SFO, SON, PVN measured by Western-blot. Data are expressed as the mean ± SD (n=15 in each group). *P<0.05 versus Non-DM.

Article Snippet: RAS activity in brain Cerebral localization of AGT and AT1 receptors was determined by double-staining immunofluorescence using anti-AGT or anti-AT1 receptors as the first primary antibody, and anti-neuron-specific enolase (Boster Biological Technology, Pleasanton, CA, USA) or anti-glial fibrillary acidic protein (Boster Biological Technology, Pleasanton, CA, USA) as the second primary antibody.

Techniques: Activity Assay, Immunohistochemistry, Western Blot

Journal: American Journal of Translational Research

Article Title: Renal and cerebral RAS interaction contributes to diabetic kidney disease

doi:

Figure Lengend Snippet: Localization of central AGT and AT1 receptors and Blood brain barrier permeability. A. Localization of central AGT and AT1 receptors determined by doublestaining with the antibodies against AGT or AT1 receptors (green) and the antibodies-recognized NSE or GFAP (red). NSE, neuron-specific enolase; GFAP, glial fibrillary acidic protein. B. Blood brain barrier permeability was up-regulated in DM rats (b1), but there was no significant difference in all intervention groups (b2).

Article Snippet: RAS activity in brain Cerebral localization of AGT and AT1 receptors was determined by double-staining immunofluorescence using anti-AGT or anti-AT1 receptors as the first primary antibody, and anti-neuron-specific enolase (Boster Biological Technology, Pleasanton, CA, USA) or anti-glial fibrillary acidic protein (Boster Biological Technology, Pleasanton, CA, USA) as the second primary antibody.

Techniques: Permeability

Journal: American Journal of Translational Research

Article Title: Renal and cerebral RAS interaction contributes to diabetic kidney disease

doi:

Figure Lengend Snippet: Expression of RAS components, NOXs and TH in brain nuclei and kidney measured by western-blot. A. Protein levels of AGT (a1) and AT1 receptors (a2) in brain nuclei measured by Western-blot. B. Protein levels of NOX2 (b1) and NOX4 (b2) in brain nuclei measured by Western-blot. C. Protein expression of TH in SFO, SON PVN (c1) and RVLM (c2) measured by western-blot. D. Protein levels of AGT, AT1, MCP-1 (d1) and Noxs (d2) in renal cortex homogenates measured by Western-blot. Data are expressed as the mean ± SD (n=6 in each group). *P<0.05 versus IG 0 mg/kg/d Los.

Article Snippet: RAS activity in brain Cerebral localization of AGT and AT1 receptors was determined by double-staining immunofluorescence using anti-AGT or anti-AT1 receptors as the first primary antibody, and anti-neuron-specific enolase (Boster Biological Technology, Pleasanton, CA, USA) or anti-glial fibrillary acidic protein (Boster Biological Technology, Pleasanton, CA, USA) as the second primary antibody.

Techniques: Expressing, Western Blot

Journal: American Journal of Translational Research

Article Title: Renal and cerebral RAS interaction contributes to diabetic kidney disease

doi:

Figure Lengend Snippet: The central administration of losartan or tempol prevented renal RAS activation. A. The central administration of losartan or tempol prevented renal RAS activation. Representative photographs and semiquantitative data of AGT, AT1 and MCP-1 expression by immunohistochemistry. B. The central administration of losartan or tempol did not prevente glomerularsclerosis, however only oral administration of drugs could alleviate glomerulosclerosis. Representative photographs and semiquantitative data of glomerulosclerosis index were shown by PAS. Data are expressed as the mean ± SD (n=6 in each group). *P<0.05 versus IG 0 mg/kg/d Los. PAS, periodic acid-Schiff.

Article Snippet: RAS activity in brain Cerebral localization of AGT and AT1 receptors was determined by double-staining immunofluorescence using anti-AGT or anti-AT1 receptors as the first primary antibody, and anti-neuron-specific enolase (Boster Biological Technology, Pleasanton, CA, USA) or anti-glial fibrillary acidic protein (Boster Biological Technology, Pleasanton, CA, USA) as the second primary antibody.

Techniques: Activation Assay, Expressing, Immunohistochemistry

Journal: Scientific Reports

Article Title: Sniffer cells for the detection of neural Angiotensin II in vitro

doi: 10.1038/s41598-019-45262-4

Figure Lengend Snippet: ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of ANG III induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.

Article Snippet: Carbachol (50 µM), Angiotensin 1–7 (0.1–100 nM), Bradykinin (0.1–100 nM), and Losartan (10 µM) were purchased from Tocris (Minneapolis, MN) and Angiotensin III (0.1–100 nM) was purchased from Alomone Labs (Jerusalem, Israel).

Techniques: Fluorescence, Transfection