annexin a1 anxa1 shrna (OriGene)
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annexin a1 anxa1 shrna
Annexin A1 Anxa1 Shrna, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/vector+a1/pRFP-C-shLenti+shRNA+Vector/pmc12905670-31-17-25
Average 94 stars, based on 6 article reviews
Annexin A1 Anxa1 Shrna, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/vector+a1/pRFP-C-shLenti+shRNA+Vector/pmc12905670-31-17-25
Average 94 stars, based on 6 article reviews
annexin a1 anxa1 shrna - by Bioz Stars,
2026-11
94/100 stars
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1) Product Images from "Myeloid cell-specific β2-adrenergic receptor deletion improves early cardiac injury resolution via de-repression of Anxa1"
Article Title: Myeloid cell-specific β2-adrenergic receptor deletion improves early cardiac injury resolution via de-repression of Anxa1
Journal: Theranostics
doi: 10.7150/thno.123651
Figure Legend Snippet: Annexin A1 expression is increased in β2AR-deficient myeloid cells post-MI. (A) RT-qPCR screening of various efferocytosis pathway genes was performed on total RNA isolated from whole bone marrow (BM) cells from FL/FL and LB2 mice, with the heatmap representing the differential expression pattern of Anxa1, Mertk, Axl, Stab1 and Stab2 genes between FL/FL and LB2 BM cells. RT-qPCR-detected Anxa1 expression in Veh or ISO-treated (10 µM for 16h) FL/FL versus LB2 BMDM (B, n = 3 each), prepared as described in Figure A. (C) Schematic of magnetic microbead column-based cardiac CD11b+ cell enrichment at 1 Day post-MI, after which gene expression of β2AR and Anxa1 were assessed via RT-qPCR (D), n = 3/group. Flow cytometry-based histogram analysis showing comparative AnxA1 protein expression via mean fluorescence intensity (MFI) among various phenotypically distinct myeloid cell types: general CD11b+ myeloid cells (E), Nu (F), Ly6C hi Mo (G), Mac (H) and Ly6C lo Mo (I) at 4 days post-MI FL/FL and LB2 hearts, n = 5/group. Data are Mean ± SEM of independent experiments. ns, non-significant, * p < 0.05; ** p < 0.01, **** p < 0.0001, Unpaired student's t-test.
Techniques Used: Expressing, Quantitative RT-PCR, Isolation, Quantitative Proteomics, Gene Expression, Flow Cytometry, Fluorescence
Figure Legend Snippet: β2AR signaling induces miR-374b-50-mediated repression of Anxa1. RT-qPCR screening of miR-196b (A, n = 4 each), miR-374b-5p (B, n = 3 each), miR-128a (C, n = 3 each) and miR-26a (D, n = 3 each) in BMDM treated with vehicle (0.002% L-ascorbic acid) or ISO (10 μM, 16h). RT-qPCR screening of miR-196b (E), miR-374b-5p (F), miR-128a (G) and miR-26a (H) in 4 day post-MI cardiac CD11b + cells, n = 5 FL/FL and n = 4 LB2. For each replicate, a minimum of 5 heart cells were combined. (I) Table showing sequence % identity between mouse (prefixed; mmu-) and human (prefixed; hsa-) miR-374b-5p. (J) Predicated alignment of miR-374b-5p with 3'-UTR of Anxa1. (K) TaqMan TM based RT-qPCR analysis of the effect of miR-374b-5p mimic on miR-374b-5p expression in HEK293T cells. (L) RT-qPCR analysis of the effect of miR-374b-5p mimic on ANXA1 gene expression in HEK293T cells. Data are Mean ± SEM of independent experiments. ns, non-significant, * p < 0.05, ** p < 0.01, *** p < 0.001, One way ANOVA with Tukey's post-hoc test (A-D, K) or Unpaired student's t-test (E-H).
Techniques Used: Quantitative RT-PCR, Sequencing, Expressing, Gene Expression
Figure Legend Snippet: Anxa1 downregulation reduces efferocytosis and ameliorative cardiac remodeling effects in myeloid cell-specific β2AR knockout mice. (A) BMDM underwent lentivirus transduction of various clones (A-D) of AnxA1 shRNA versus control (CTL) shRNA for 48 h, after which RT-qPCR was used to assess gene silencing efficiency, n = 3/group. (B) Schematic depicting the experimental design to test the impact of AnxA1 knockdown in LB2 bone marrow-derived Nu. Briefly, LB2 BM cells were transduced with lentivirus containing either CTL shRNA or AnxA1 shRNA (1:1 mixture of clones B and D), after which they were retro-orbitally injected into lethally irradiated LB2 mice to generate bone marrow transplant (BMT) mice featuring LB2 bone marrow with or without AnxA1 knockdown, as confirmed via RT-qPCR analysis after terminal experiments (C), n = 4 (CTL shRNA), n = 4 (AnxA1 shRNA). 4 weeks after BM reconstitution, CTL shRNA and AnaA1 shRNA Nu were enriched from the respective BMT mice using magnetic columns, after which they underwent efferocytosis assays with LB2 BMDM (as described in Figure ) and flow cytometry analysis, as shown via contour plots (D) of LB2 BMDM incubated without Nu (left) or with CMFDA + Nu from either CTL shRNA (middle) or Anxa1 shRNA (right) LB2 BMT mice. (E) Quantification of CTL shRNA versus Anxa1 shRNA LB2 Nu uptake efficiency into LB2 BMDM in terms of % efferocytosis, n = 4/each group. CTL shRNA and AnxA1 shRNA-transduced LB2 BMT mice were generated as described above and 4 weeks after BM reconstitution underwent MI surgery. Histograms depicting %EF (F) and %FS (G) at baseline, 3 and 14 days post-MI in CTL and AnxA1 shRNA LB2 BMT mice, n = 4 for CTL, n = 6 for AnxA1 shRNA. (H) MT staining of whole heart (top row) displaying infarct size of CTL and AnxA1 shRNA LB2 BMT mice at 14 days post-MI with quantification shown in (I), n = 4 for CTL and n = 5 for AnxA1 shRNA group, scale bar = 1000 µm, and 20X images (bottom row) displaying interstitial fibrosis in the border zone of the post-MI hearts with quantification as % area fibrosis (J), n =4 for CTL and n = 5 for AnxA1 shRNA group, scale bar = 100 µm. Data are Mean ± SEM of independent experiments. ns, non-significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, One way ANOVA with Tukey's post-hoc test (A), Unpaired student's t-test (C, E, I, J) or Two-way repeated measures ANOVA with Tukey's post-hoc test (F, G).
Techniques Used: Knock-Out, Transduction, Clone Assay, shRNA, Control, Quantitative RT-PCR, Knockdown, Derivative Assay, Injection, Irradiation, Flow Cytometry, Incubation, Generated, Staining
Figure Legend Snippet: Mechanism of myeloid cell-specific β2AR deletion-mediated post-MI injury resolution. Myocardial infarction triggers local ischemic damage and elevated catecholamines (epinephrine/norepinephrine; NE/EP). Stimulation of myeloid cell β2AR increases the abundance of miR-347b-5p leading to degradation of Anxa1 mRNA, resulting in decreased Anxa1 protein expression (A). In the absence of β2AR, miR-347b-5p cannot be induced, leading to de-repression of Anxa1 expression, and ultimately increased Nu efferocytosis (B). This enhanced Nu clearance during the early post-MI period leads to better injury resolution with less fibrosis and infarct expansion and better contractile function.
Techniques Used: Expressing
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