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. Author manuscript; available in PMC: 2020 Aug 22.
Published in final edited form as: Cell. 2019 Aug 8;178(5):1231–1244.e11. doi: 10.1016/j.cell.2019.07.033

Figure 4. Blockade of GDF15 in acute inflammatory states results in defects cardiac and thermal homeostasis.

Figure 4.

(A) Plasma troponin I levels 24 and 36 hours after either LPS or Poly(I:C) injection following pre-treatment with either isotype or α-GDF15 antibody.

(B) Plasma creatinine levels 24 and 36 hours after either LPS or Poly(I:C) injection following pre-treatment with either isotype or α-GDF15 antibody.

(C) Plasma blood urea nitrogen (BUN) levels 24 and 36 hours after either LPS or Poly(I:C) injection following pre-treatment with either isotype or α-GDF15 antibody.

(D) Plasma alanine aminotransferase (ALT) levels 24 and 36 hours after either LPS or Poly(I:C) injection following pre-treatment with either isotype or α-GDF15 antibody.

(E) Cxcl1, Tnf, Il12b, Mx1 expression levels in heart tissue 8 hours after injection of either LPS or Poly(I:C) following pre-treatment with either isotype or α-GDF15 antibody. Abundance is relative to Rpl13a expression.

(F) Stroke volume as measured by trans-thoracic echocardiogram 24 hours after LPS injection following pre-treatment with either isotype or α-GDF15 antibody.

(G) Cardiac output calculated from trans-thoracic echocardiogram measurements 24 hours after LPS injection following pre-treatment with either isotype or α-GDF15 antibody.

(H) Rectal temperature in mice 20 hours after LPS injection following pre-treatment with either isotype or α-GDF15 antibody.