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Table 2 Studies of Pax3/Pax7 using in vitro and in vivo models

From: The regenerative potential of Pax3/Pax7 on skeletal muscle injury

 

Results

Reference

In vitro

Cell line

 Cell from muscle tissue of mutated mice (Pax3nLacZ/+ and Pax7LacZ/+ mice)

Progressive loss of Pax7 leads to satellite cell death during the cell cycle

[41]

 Primary myoblast cells

In mature myoblasts, Pax3 binds to several subsets of Pax7 targets and thus has overlapping functions in the transcriptional network

[48]

 iPax7 cells {pluripotent stem cells (PSC)}

Pax7 binding induces chromatin remodelling characterised by histone markers related to enhancers and acceptance of chromatin availability in PSCs

[53]

In vivo

Animal

 Young mice were injected with siRNA

Studies have shown that H3K4 is deactivated by the knockdown of Pax3/Pax7 binding protein and restrains the multiplication of muscle precursor cells (MPCs). Therefore, the Pax3/Pax7 binding protein becomes the adapter that connects the Pax3/Pax7 with the H3K4 HMT

[49]

 Mice were injected by ESCs (WT/KO of Pax7)

Initiation of myogenic differentiation is facilitated while Pax7 is absent

[54]

 Mice were injected with TCDD

Pax3/Pax7 is needed to guard against TCDD (pollution)

[55]

 Pax7 gene deprived mice (Pax7−/− mice)

Pax3+ in muscle interstitials expresses MyoD during regeneration, and Pax7 functions in developing utilitarian myogenic progenitors from sublaminar satellite cells

[56]

 Pax3GFP/null mice crossing with Pax3GFP/+ mice

miR-27b directs Pax3 protein levels, and this guideline guarantees a quick and vigorous section into the myogenic separation programme

[57]

 Mouse mutant

Pax + elicits muscle progenitors. There is no skeletal muscle; the mice experienced apoptosis after down-regulation of Pax7

[58]

  1. WT Wildtype, KO Knocked-out, TCDD 2,3,7,8-tetrachlorodibenzo-p-dioxin