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Growth failure in cystic fibrosis (CF) patients has been well-documented and shown to correlate with poorer disease outcomes. This observation is also true in CF animal models, including mouse, pig, rat, and ferret. The etiology underlying growth deficits is unknown, and our previous work demonstrated reduced tubulin acetylation in CF cell models and tissue that is correctable by inhibition of histone deacetylase-6 (HDAC6). Here, we hypothesize that loss of HDAC6 will improve growth phenotype in a CF mouse model.  Hdac6  knockout mice were crossed with  F508del  (CF) mice to generate  F508del / Hdac6  (CF/HDA) mice. Growth, fat deposits, survival, and bioelectric measurements were analyzed.  CF / HDA  mice displayed improvements in length and weight with no correction of CFTR function. Mechanistically,  Igf1  levels likely account for increased length and improvements in fertility. Weight gain is attributed to increased fat deposits potentially mediated by increased adipocyte differentiation. CF-related growth deficits can be improved via inhibition of HDAC6, further implicating it as a potential therapeutic target for CF.

Improved Growth Patterns in Cystic Fibrosis Mice after Loss of Histone Deacetylase 6