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Peripheral nerve injury is common, and can lead to skeletal muscle atrophy and dysfunction. However, the underlying molecular mechanisms are not fully understood. The transcription factors have been proved to play a key role in denervated muscle atrophy. In order to systematically analyze transcription factors and obtain more comprehensive information of the molecular regulatory mechanisms in denervated muscle atrophy, a new transcriptome survey focused on transcription factors are warranted. In the current study, we used microarray to identify and analyze differentially expressed genes encoding transcription factors in denervated muscle atrophy in a rat model of sciatic nerve dissection. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were used to explore the biological functions of differentially expressed transcription factors and their target genes related to skeletal muscle pathophysiology. We found that the differentially expressed transcription factors were mainly involved in the immune response. Based on correlation analysis and the expression trends of transcription factors, 18 differentially expressed transcription factors were identified. Stat3, Myod1, Runx1, Atf3, Junb, Runx2, Myf6, Stat5a, Tead4, Klf5, Myog, Mef2a, and Hes6 were upregulated. Ppargc1a, Nr4a1, Lhx2, Ppara, and Rxrg were downregulated. Functional network mapping revealed that these transcription factors are mainly involved in inflammation, development, aging, proteolysis, differentiation, regeneration, autophagy, oxidative stress, atrophy, and ubiquitination. These findings may help understand the regulatory mechanisms of denervated muscle atrophy and provide potential targets for future therapeutic interventions for muscle atrophy following peripheral nerve injury.

Yuanyuan Wang,1,2,* Hua Wang,3,* Jian Zhang,2 Zhifen Chu,2 Pu Liu,2 Xing Zhang,2 Chao Li,2 Xiaosong Gu1 1Academy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin, People’s Republic of China; 2Department of General Surgery, Hebei Key Laboratory of Colorectal Cancer Precision Diagnosis and Treatment, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China; 3Department of Pharmacy, Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China*These authors contributed equally to this workCorrespondence: Chao LiDepartment of General Surgery, Hebei Key Laboratory of Colorectal Cancer Precision Diagnosis and Treatment, The First Hospital of Hebei Medical University, Shijiazhuang 050031, Hebei, People’s Republic of ChinaEmail zxp10au@163.comXiaosong GuAcademy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin 300072, People’s Republic of ChinaTel +86-0311-85917000Email kfewbf@163.comBackground: Colorectal cancer (CRC) is a kind of malignant tumor, and the development of chemoradiotherapy resistance (CRR) increases the difficulty of its treatment. The role of circular RNAs (circRNAs) in cancer progression has been well documented. Nevertheless, the function of circ_0007031 in the growth and CRR of CRC has not been well elucidated.Methods: CRR cell lines were constructed using 5-Fu and radiation. Cell counting kit 8 (CCK8) assay was employed to measure the 5-Fu resistance and proliferation of cells. Clonogenic assay was used to evaluate the radiation resistance of cells. Also, the expression of circ_0007031 and microRNA-760 (miR-760) was determined using quantitative real-time polymerase chain reaction (qRT-PCR). The cell cycle distribution and apoptosis of cells were assessed by flow cytometry. Besides, the levels of apoptosis-related protein and mRNA-decapping enzyme 1a (DCP1A) protein were measured by Western blot (WB) analysis. Further, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were used to confirm the interaction between miR-760 and circ_0007031 or DCP1A. In addition, animal experiments were performed to evaluate the function of silenced circ_0007031 on the 5-Fu and radiation resistance of CRC tumors.Results: Circ_0007031 expression was markedly increased in CRC tissues and cells, especially in CRC resistant cells. Circ_0007031 knockdown hindered proliferation, induced cell cycle arrest in the G0/G1 phase, enhanced apoptosis, and lowered the CRR of CRC resistant cells. Further, miR-760 could be targeted by circ_0007031, and its inhibitor could reverse the inhibition effect of circ_0007031 knockdown on the growth and CRR of CRC resistant cells. Moreover, DCP1A was a target of miR-760, and its overexpression could invert the suppression effect of miR-760 overexpression on the growth and CRR of CRC resistant cells. Circ_0007031 silencing could enhance the sensitivity of CRC tumors to 5-Fu and radiation to markedly reduce CRC tumor growth in vivo.Conclusion: Circ_0007031 might play a positive role in the CRR of CRC through regulating the miR-760/DCP1A axis, which might provide a new approach for treating the CRR of CRC.Keywords: colorectal cancer, CRR, circ_0007031, miR-760, DCP1A

Prior research generally confirms that there are no neuronal cell bodies in the adult sciatic nerve. However, we occasionally find some neuronal cells in adult rat sciatic nerves, either intact or crush-injured. By whole-mount staining and optical imaging of the hyalinized sciatic nerves for Stmn2 (a specific marker for neuronal cells), we found those neuronal cells with irregular distribution in the sciatic nerves in both crushed model and normal rats. We investigated the identity of those cells and established a cultured sciatic nerve model. Immunohistochemistry evidence both in vivo and in vitro illustrated that some of those cells are mature neurons in sciatic nerves. With single-cell sequencing of neuronal cells in adeno-associated virus (AAV)-infected sciatic nerves, we identified that some of those cells are a kind of neuronal stem-like cells. Then we constructed a Nestin-CreERT2 rat line and traced those cells with fluorescence labeling which was induced by tamoxifen. Interesting, we proved that neuronal stem-like cells could proliferate by combination of EdU incorporation with staining in the sciatic nerves of transgenic rats. Together, the discovery of neuronal cells in adult sciatic nerves will make us aware of the distribution of neurons in the peripheral nervous system. Especially our data suggest that neuronal stem-like cells could proliferate in the sciatic nerves of adult rats.

Schwann cells (SCs) play an essential role in nerve injury repair. A striking feature of the cellular response to peripheral nerve injury is the proliferation of SCs. Circular (circ)RNAs are enriched in the nervous system and are involved in physiologic and pathologic processes. However, the potential role of circRNAs in SC proliferation post nerve injury remains largely unknown. Using a sciatic nerve crush model, we obtained an expression profiling of circRNAs in injured sciatic nerves in rats by RNA sequencing and bioinformatics analysis, and we further identified a circRNA [circ–ankyrin repeat and in-between Ring finger (IBR) domain containing 1 (Ankib1)] involved in SC proliferation by the transfection of specific small interfering RNAs. Overexpression of circ-Ankib1, which was specifically and highly enriched in SCs, impaired SC proliferation and axon regeneration following sciatic nerve injury. Mechanistically, increased expression of DEx/H-box helicase 9 (DHX9) postinjury might contribute to the down-regulation of circ-Ankib1, which further suppressed cytochrome P450, family 26, subfamily B, polypeptide 1 expression by sponging miR-423-5p, miR-485-5p, and miR-666-3p, leading to the induction of SC proliferation and nerve regeneration. Taken together, our results reveal a crucial role for circRNAs in regulating proliferation of SCs involved in sciatic nerve regeneration; as such, circRNAs may serve as a potential therapeutic avenue for nerve injury repair.—Mao, S., Zhang, S., Zhou, S., Huang, T., Feng, W., Gu, X., Yu, B. A Schwann cell–enriched circular RNA circ-Ankib1 regulates Schwann cell proliferation following peripheral nerve injury.

In this study, the effects of carbon quantum dot (CQD) doping on the photocatalytic performance of semiconductor BiOCl microspheres were investigated. Highly dispersed CQDs with up-conversion luminescence properties were prepared using the hydrothermal method, and visible-light-responsive CQDs@BiOCl photocatalysts with regular morphology were prepared via CQD doping. Scanning electron microscopy (SEM), energy dispersive spectroscopy (EDS), transmission electron microscopy (TEM), X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS) and ultraviolet–visible (UV–Vis) spectroscopy were used to investigate the morphology and light absorption properties of the materials. The degradation rate of rhodamine B (RhB) was 76.1% after 180 min of visible-light irradiation when CQDs@BiOCl were used and only 19.4% when pure BiOCl was used. The photoluminescence (PL), UV–Vis diffuse reflectance spectra (UV–Vis DRS) and electron paramagnetic resonance (EPR) results were analyzed to determine the possible reasons for the increased photocatalytic activity of CQDs@BiOCl microspheres. The results showed CQD doping expanded the visible light absorption range, CQDs exhibited fast photoinduced electron transfer, and CQDs@BiOCl possessed high mesoporosity, which promoted the effective separation of photogenerated electron–hole pairs. In addition, the microsphere structure of CQDs@BiOCl exhibited a larger specific surface area and a more regular morphology than its sheet-like structure. These features increased the number of photocatalytic reaction sites and the surface adsorption of the catalyst. In addition, the electronic conjugated structure of CQDs was demonstrated to function as an effective electron trap. CQD doping effectively inhibited the photogenerated electron–hole pair recombination of the composite photocatalyst, which enhanced the photocatalytic performance of the system.

The effect of noble metal silver (Ag) modification on the photocatalytic performance of layered BiOCl microspheres was investigated herein. BiOCl@Ag, a visible-light-responsive photocatalyst with regular morphology, was prepared via a solvothermal method using BiOCl. Scanning electron microscopy, energy dispersive spectroscopy, transmission electron microscopy, X-ray diffraction, X-ray photoelectron spectroscopy and ultraviolet–visible spectroscopy were used to investigate the morphology and light absorption properties of the materials. The degradation rate of RhB was 88.2% after 90 min of visible-light irradiation when BiOCl@Ag was used and only 32.4% when pure BiOCl was used. Photoluminescence and electron spin resonance studies were conducted to determine why the use of BiOCl@Ag resulted in higher photocatalytic activity than the use of pure BiOCl. The results showed the surface plasmon resonance effect of BiOCl@Ag extended the range of visible light absorption. Furthermore, a Schottky barrier was used as a photoelectron capture center to promote the effective separation of photogenerated charges. Finally, the interaction of noble metals and semiconductors increased the activity of oxidizing free radicals on the catalyst surface. This study showed the Ag loading of BiOCl effectively improved the photocatalytic performance of BiOCl.