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: Molecular Nutrition & Food Research

Article Title: Chlorogenic Acid Ameliorates Chronic Unpredictable Stress‐Induced Diminished Ovarian Reserve Through Ovarian Renin‐Angiotensin System

doi: 10.1002/mnfr.202400814

Figure Lengend Snippet: CGA improved DOR by reducing oxidative stress and apoptosis levels in mouse ovaries through its effects on the ACE‐AngII‐AT1R axis. (A) and (B) The qRT‐PCR analysis of the OVRAS components Ace , Agt , Agtr1a , Agtr1b , Ace2 , Agtr2 , and MasR ( n = 3). (C) Expression levels of oxidative stress and apoptosis molecular markers ( Bax , Bcl‐2 , Sod2 , and Gpx4 ) in the ovaries were detected by qRT‐PCR ( n = 3). (D–F) Quantification of ACE, AGT, AGTR1, ACE2, AGTR2, MasR, BAX, Bcl‐2, SOD2, and GPX4 protein expression. (G) and (H) Photographs of western blot showing the protein level of ACE, ACE2, AGT, AGTR1, AGTR2, MasR, BAX, Bcl‐2, GPX4, and SOD2. (I) and (J) Analysis of AngII and Ang(1‐7) in mouse ovary tissue homogenates collected from each group ( n = 3). CAT (K), GSH (L), and MDA (M) levels as oxidative stress indicators were determined in mouse ovary tissue homogenates ( n = 6). Results are expressed as the mean ± SD and one way ANOVA was used for between‐group comparisons, n represents the number of biological replicates. * p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant.

Article Snippet: Proteins were separated on SDS‐PAGE gels (Epizyme, China), transferred to PVDF membranes (Millipore, USA), and then blocked with 5% non‐fat milk at room temperature for 2 h. The following primary antibodies were used: AGT (Affinity, China, DF7976, 1:1000), AGTR1 (BOSTER, China, BM4949, 1:1000), AGTR2 (BOSTER, China, BM4557, 1:1000), MasR (Affinity, China, DF2818, 1:1000), ACE (Affinity, China, AF5197, 1:1000), ACE2 (Affinity, China, AF5165, 1:1000), BAX (Bimake, USA, A5131, 1:1000), Bcl‐2 (Affinity, China, BF9103, 1:1000), SOD2 (Selleck, USA, A5377, 1:1000), GPX4 (Selleck, USA, A5569, 1:1000), GAPDH (Proteintech, China, 60004‐1‐Ig, 1:10000).

Techniques: Quantitative RT-PCR, Expressing, Western Blot

Journal: Molecular Nutrition & Food Research

Article Title: Chlorogenic Acid Ameliorates Chronic Unpredictable Stress‐Induced Diminished Ovarian Reserve Through Ovarian Renin‐Angiotensin System

doi: 10.1002/mnfr.202400814

Figure Lengend Snippet: CGA decreased activity of ACE‐AngII‐AT1R axis as well as reduced oxidative stress and apoptosis levels of Dex‐induced KGN cells. (A) and (B) The qRT‐PCR analysis of OVRAS components ACE , AGT , AGTR1 , ACE2 , AGTR2 , and MasR mRNA expression level ( n = 3). (C) Expression levels of oxidative stress and apoptosis molecular markers ( BAX , Bcl‐2 , SOD2 , and GPX4 ) detected by qRT‐PCR ( n = 3). (G) and (H) The OVRAS, oxidative stress and apoptosis‐related protein expression in PVDF membrane. (D) and (E) Quantification of ACE, AGT, AGTR1, ACE2, AGTR2, and MasR protein expression ( n = 3). (H) Quantification of BAX, Bcl‐2, SOD2, and GPX4 protein expression ( n = 3). Results are expressed as the mean ± SD and one way ANOVA was used for between‐group comparisons, n represents the number of biological replicates. * p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant.

Article Snippet: Proteins were separated on SDS‐PAGE gels (Epizyme, China), transferred to PVDF membranes (Millipore, USA), and then blocked with 5% non‐fat milk at room temperature for 2 h. The following primary antibodies were used: AGT (Affinity, China, DF7976, 1:1000), AGTR1 (BOSTER, China, BM4949, 1:1000), AGTR2 (BOSTER, China, BM4557, 1:1000), MasR (Affinity, China, DF2818, 1:1000), ACE (Affinity, China, AF5197, 1:1000), ACE2 (Affinity, China, AF5165, 1:1000), BAX (Bimake, USA, A5131, 1:1000), Bcl‐2 (Affinity, China, BF9103, 1:1000), SOD2 (Selleck, USA, A5377, 1:1000), GPX4 (Selleck, USA, A5569, 1:1000), GAPDH (Proteintech, China, 60004‐1‐Ig, 1:10000).

Techniques: Activity Assay, Quantitative RT-PCR, Expressing, Membrane

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: 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