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. Author manuscript; available in PMC: 2023 Feb 1.
Published in final edited form as: Cell Metab. 2022 Feb 1;34(2):299–316.e6. doi: 10.1016/j.cmet.2021.12.019

Figure 4. Erythrocyte TG2 deletion exacerbates Ang II-induced CKD manifestations and disturbs L-carnitine-dependent renal metabolism.

Figure 4.

a. Systolic blood pressure (BP) was measured on days 0, 3, 7 and 14 of Ang II infusion. *P<0.05, Saline versus Ang II (n=4–6). kits. *P<0.05, (n=4–6).

b. Urinary protein, plasma creatinine and plasma urea were quantified by commercially available kits. *P<0.05, (n=4–6).

c. Top panel: Representative images of hypoxyprobe staining in kidney, heart and liver (scale bar=100 μm). Bottom panels: Representative images of Masson’s trichrome staining in kidney,heart and liver (scale bar=200 μm). *P<0.05 (n=4).

d. Representative hematoxylin and eosin (H&E) staining of sections of kidney cortex (scale bar=200 μm). *P<0.05, (n=4).

e. Experimental design for mouse sample collection and metabolomics study.

f. Untargeted metabolomics screening data indicated L-carnitine and acyl-carnitine loss in kidney, erythrocyte (RBC) and plasma, (n=3–5).

g. Urine L-carnitine fold change of Tgm2f/f EpoR-Cre+ + Ang II versus EpoR-Cre+ mice + Ang II.

h. Protein levels of OCTN2 in kidneys and erythrocyte membranes. All data are expressed as mean ± SD and were analyzed by two-way ANOVA followed with Sidak’s multiple comparisons test. See also Figure S4 and Table S2.