Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Jun 18;11:12903. doi: 10.1038/s41598-021-92303-y

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Col4a1/a2 is required to maintain VSMCs in the contractile phenotype. (a) Number of proteins identified in unchallenged aortas and proximal halves of AAA lesions, and the number of regulated proteins (uncorrected p ≤ 0.05) by the Col4a1/a2^+/− genotype for each condition. For unchallenged aortas, we analyzed 40 samples (aortas from 10 female Col4a1/a2^+/+ mice, 12 female Col4a1/a2^+/− mice, 9 male Col4a1/a2^+/+ mice, and 9 male Col4a1/a2^+/− mice) mixing sexes to increase statistical power. For AAA lesions, we analyzed 28 samples (AAA from 13 male Col4a1/a2^+/+ mice and 15 male Col4a1/a2^+/− mice). (b) Significantly regulated proteins in unchallenged aortas after correction for multiple testing (fdr ≤ 0.05). No proteins remained significantly regulated for AAA lesions after correction for multiple testing. (c) Significantly enriched GO terms among the 94 downregulated proteins (uncorrected p ≤ 0.05, excluding Col4a1/a2) in unchallenged Col4a1/a2^+/− aortas. No GO terms were significantly regulated for upregulated proteins (uncorrected p ≤ 0.05) in unchallenged aortas, or up- or down-regulated proteins (uncorrected p ≤ 0.05, excluding Col4a1/a2) in AAA lesions. (d) Volcano plot showing protein level changes in unchallenged Col4a1/a2^+/− aortas relative to Col4a1/a2^+/+ aortas. Col4a1/a2 (red), VSMC markers²⁹ (magenta), BM proteins (yellow), and non-BM collagens (grey) are magnified for clarity. Identities of regulated (uncorrected p ≤ 0.05) VSMC markers and BM proteins are shown in the parallel shifted rectangle. (e) Volcano plot showing protein level changes in Col4a1/a2^+/− AAA lesions relative to Col4a1/a2^+/+ lesions. The color code of magnified dots is the same as in (d). For (d, e), the red horizontal lines show the corrected (fdr = 0.05) and uncorrected (p = 0.05) level of significance, respectively. Data in (b) and (d, e) were analyzed by unpaired t-test for each protein followed by fdr correction for multiple testing.