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. 2009 Nov 2;106(46):19599–19604. doi: 10.1073/pnas.0907935106

Fig. 2.

Fig. 2.

Pharmacological inhibitors selective for HDAC6 are protective in oxidatively stressed neurons, and promote neurite outgrowth in the presence of MAG. (A) Neuronal viability after treatment with homocysteic acid (HCA; 5 mM) with or without the pan-HDAC inhibitor TSA (0.66 μM), or the HDAC6-selective inhibitors MA-I (10 μM), and MA-II (10 μM) for 24 h. Viability was measured by using MTT assay. *, Significant protection compared to HCA treatment alone P < 0.001. §, Significant death compared to non-HCA control P < 0.001. (B) Live/Dead staining of treated rat primary cortical cultures. (C and D) Mean neurite length of cortical neurons measured after 24 h coculture with either R2 and R2M21+MAG cells in the presence or absence of the RhoA kinase Inhibitor (ROCKI), Y27632 (10 μM), the pan-HDAC inhibitor, TSA, or the HDAC6-selective inhibitors MA-I, and MA-II. Neurites were identified by neuron-specific β-III tubulin immunostaining and fluorescence microscopy (D), and measured by using Metamorph (C). Significant increase in neurite length relative to nontreated R2M21+MAG denoted by *, P < 0.05 or **, P < 0.001. Significant increase in neurite length relative to nontreated R2 denoted by §, P < 0.05.