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. 2022 Aug 8;11(1):487–500. doi: 10.1080/21623945.2022.2108558

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© 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 8. — PDE4B depletion enhanced cAMP/PKA signalling and lipophagy. Mature adipocytes infected with lentiviruses carrying PDE4B shRAN or control were treated with or without 100 nM of autophagic inhibitor bafilomycin A1 (BFA) and/or 1 μM of PKA inhibitor PKI for 24 h. (a) Effect of PDE4B depletion on the intracellular cAMP concentration. (b) Effect of PDE4B depletion on the intracellular PKA activity. (c) Effect of PDE4B depletion on the protein or phosphorylated protein levels of CREB, HSL, and PLIN 1. (d) Effect of PDE4B depletion on the protein levels of beclin 1 and LC3. (e) Effects of BFA and PKI on cAMP/PKA signalling and lipophagy in PDE4B KD cells. (f) Effects of BFA and PKI on glycerol concentration in culture medium in PDE4B KD cells. (g) Effect of BFA on lipophagy and UCP1 protein levels in PDE4B KD cells. (h) Effect of PKI on UCP1 protein levels in PDE4B KD cells. Data are presented as mean ± SD, n = 3; *p < 0.05, **p < 0.01, ***p < 0.001 vs indicated group. KD: knockdown; CNTL: control; ns: no significant.