miR-33-3p Regulates PC12 Cell Proliferation and Differentiation In Vitro by Targeting Slc29a1

Author(s):  
Bo-Quan Shan ◽  
Wen Li ◽  
Hui He ◽  
He-Yan Zhao ◽  
Mei-Ling Tian ◽  
...  
1995 ◽  
Vol 15 (7) ◽  
pp. 3470-3478 ◽  
Author(s):  
R Hopewell ◽  
E B Ziff

Heterodimerization of Max with the nuclear oncoprotein Myc and the differentiation-associated proteins Mad and Mxi1 enables these factors to bind E-box sites in DNA and control genes implicated in cell proliferation and differentiation. We show that in the PC12 pheochromocytoma tumor cell line, functional Max protein is not expressed because of the synthesis of a mutant max transcript. This transcript encodes a protein incapable of homo- or heterodimerization. Furthermore, the mutant Max protein, unlike wild-type Max, is incapable of repressing transcription from an E-box element. Synthesis of mutant max transcripts appears to be due to a homozygous chromosomal alteration within the max gene. Reintroduction of max into PC12 cells results in repression of E-box-dependent transcription and a reduction in growth rate, which may explain the loss of Max expression either during the growth of the pheochromocytoma or in subsequent passage of the PC12 cell line in vitro. Finally, the ability of these cells to divide, differentiate, and apoptose in the absence of Max demonstrates for the first time that these processes can occur via Max- and possibly Myc-independent mechanisms.


2020 ◽  
Author(s):  
Amina El Ayadi ◽  
Melody R.S. Threlkeld ◽  
Steven E. Wolf ◽  
Juquan Song

Abstract Background: Skeletal muscle injury leads to loss of muscle function that lasts well into recovery and can be permanent. Application of the novel bio-scaffold termed porcine-derived urinary bladder matrix (UBM) has a potential benefit to mitigate injury through tissue regeneration. To date, findings of potential benefit in animal models were limited to short assessment times. The purpose of this study was to investigate whether UBM treatment 14 days after injury sustainably improves the recovery of muscle function in injured mice. Methods: C57BL/6 adult male mice received bilateral laceration injuries on the gastrocnemius (GN) muscle under anesthesia and were then treated with vehicle or 150 µg of UBM nanoparticles. Treatment was applied immediately after injury or 14 days later. Muscle isometric force was measured 60 days after injury. Previous time course analyses have shown that muscle function did not start to improve until after 42 days after injury. Therefore, we designed a second experiment to trace the time course of UBM effects on muscle function recovery by measuring the isometric muscle force at 49 and 90 days after injury. In vitro, we analyzed the effects of UBM on muscle cell proliferation and differentiation. Results: UBM promotes muscle cell proliferation and differentiation. Twitch (Pt), tetanic (Po) force and maximal fatigue were significantly decreased in the injured mice on day 60. Muscle fatigue maximum force significantly recovered when UBM treatment was applied 14 days after injury (p<0.05) but not when UBM was applied immediately after the injury. Time course analysis demonstrated that UBM improvement of Pt and Po was evident by day 49 after injury (p<0.05). However, no further muscle function improvement was observed on day 90. Conclusions: Delayed treatment with the UBM improves muscle function recovery following laceration injury starting 49 days after injury. These effects may be mediated by improvements in muscle cell proliferation and differentiation. This animal model is suitable to test other therapeutic strategies to improve muscle function after injury.


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