**3.2 Chromatin architecture involvement in APAR**

Overexpressed genes in NHA astrocytes exposed to lipotoxic PA concentrations were fully integrated to ChIP-Seq data, APAR-related data and the chromatin conformation in order to identify co-regulated genomic regions in astrocytes [44]. We identified 328 molecular processes that were found overexpressed when astrocytes are exposed to PA, of which 27 molecular APAR associated processes were selected based on the role and significance (**Table 3**).

Although comparing specific TAD regions from Hi-C experiments and differentially expressed genes associated with APAR mechanisms in astrocytes, we identified clusters sharing the same TAD (**Table A1**). In this regard, we identified 3039 and 3048 TAD regions for spinal cord and cerebellum astrocytes, respectively. We focused on differentially expressed genes present among the APAR gene sets, located in the corresponding TAD regions to identify co-regulated genes or regulatory profiles. Moreover, due to the CTCF role in the conformation of chromatin folding architecture,


**Table 3.**

*Differentially expressed biological processes associated with the APAR mechanisms of PA-lipotoxicity in astrocytes. All considered processes have p > 0.05 as a threshold value of significance.*

TAD regions were overlapped with CTCF in order to identify true TAD regions. In this sense, these results elucidated some of the potential role of epigenetic modulation in the APAR molecular mechanisms in astrocytes in response to PA-lipotoxicity [45–47].
