OBJECTIVETo explore the role of microtubule-associated protein 2 (MAP-2) and nestin in the development of tongue muscles of human embryos and fetuses.

METHODSPV immunohistochemistry was used to detect the expressions of MAP-2 and nestin proteins in the tongue tissues of human embryos and fetuses at the second, third and fourth months of gestation.

RESULTSMAP-2 and nestin positivity was detected in the tongue muscles of human embryos at 2 to 4 months of gestation. In the embryos at the second month of gestation, no obvious MAP-2 positive cells were found in the tongue muscles; at 3 and 4 months, the number of MAP-2-positive cells in the tongue muscles was 24.14∓8.28 and 15.86∓3.89, with the expression intensity of 109.42∓11.62 and 124.27∓8.73, respectively. At 2, 3 and 4 months of gestation, the number of nestin-positive cells in the tongue muscles was 12.50∓3.17, 19.00∓7.63, and 22.80∓6.91, with expression intensity of 119.99∓24.02, 102.20∓11.76, and 98.24∓10.66, respectively. As the gestational age increased, the number of MAP-2-positive cell number continued to decline following a transient increase but the expression intensity kept increasing; nestin-positive cells increased continuously but the expression intensity kept decreasing in the embryonic or fetal tongue muscles.

CONCLUSIONMAP-2 and nestin proteins are involved in the regulation of the development of tongue muscles in human embryos and fetuses.

Fetus ; metabolism ; Humans ; Microtubule-Associated Proteins ; metabolism ; Nestin ; metabolism ; Tongue ; embryology ; growth & development ; metabolism

Humans ; Hypertension, Pulmonary ; metabolism ; Inhibitor of Apoptosis Proteins ; Microtubule-Associated Proteins ; metabolism

Objective: To explore the expression of autophagy related factors microtubule associated protein 1 light chain 3B (LC3B), p62, autophagy key factor Beclin1 in oral lichen planus (OLP) tissues and their relationships with the clinicopathological characteristics of OLP, investigating the function and significance of autophagy in pathogenesis of OLP. Methods: Forty-one lesion tissues (OLP group, twenty-one cases of erosive OLP and twenty cases of non-erosive OLP) were selected from OLP patients visiting the Department of Periodontal and Oral Medicine, School and Hospital of Stomatology, Guizhou Medical University from October 2017 to December 2019. Fifteen cases of normal oral mucosal tissues (control group) were collected from oral and maxillofacial surgery at The Affiliated Stomatology Hospital of Guizhou Medical University during the same period. Protein and mRNA expression levels of LC3B, p62 and Beclin1 were detected by immunohistochemistry (IHC) and real-time quantitative PCR (RT-qPCR) in OLP lesions respectively. The protein expression levels of LC3B, p62, Beclin1 and ratio of LC3B-Ⅱ/LC3B-Ⅰ in sixteen cases (eight cases of erosive OLP and eight cases of non-erosive OLP) from the OLP group were detected by Western blotting (WB). The potential relationship between LC3B, p62, Beclin1, LC3B-Ⅱ/LC3B-Ⅰ ratio and clinical features of OLP were analyzed. Results: IHC results showed that the positive expression rates of LC3B and p62 proteins in OLP lesion tissues [LC3B: 68% (28/41); p62: 59% (24/41)] were higher than those in the control group [LC3B: 5/15; p62: 3/15] (LC3B: χ²=5.55, P=0.019; p62: χ²=5.55, P=0.015). The positive expression rates of LC3B and p62 proteins in the erosive OLP group [LC3B: 86% (18/21); p62: 76% (16/21)] were higher than those in the non-erosive OLP group [LC3B: 50% (10/20); p62: 40% (8/20)] (LC3B: χ²=4.50, P=0.034; p62:χ²=5.53, P=0.019). The positive expression rate of Beclin1 protein in the OLP lesions[20% (8/41)] was lower than that in the control group (7/15) (χ²=4.13, P=0.042), but was not statistically different between the two types of OLP (P>0.05). The RT-qPCR results showed that the mRNA expression levels of LC3B and p62 in OLP lesions [LC3B: 2.78 (1.59, 6.15); p62: 4.30 (2.34, 6.29)] were higher than those in the control group [LC3B: 1.05 (0.88, 1.21); p62: 1.12 (0.89, 1.36)] (LC3B: Z=-4.56, P<0.001; p62: Z=-4.78, P<0.001), and the mRNA expression levels of LC3B and p62 in the erosive OLP group were higher than those in the non-erosive OLP group (LC3B: Z=-2.87, P=0.004; p62: Z=-2.95, P=0.003). The mRNA expression level of Beclin1 in OLP tissues was lower than that in the control group (Z=-2.43, P=0.015), but the difference was not statistically significant between the two types of OLP (P>0.05). WB results showed that the LC3B-Ⅱ/LC3B-Ⅰ ratio was higher in the OLP lesions than that in the control group (t=-2.45, P=0.021), and the LC3B-Ⅱ/LC3B-Ⅰ ratio was higher in the non-erosive OLP group than in the erosive OLP group (t=-2.38, P=0.032). Spearman's correlation analysis showed that the ratio was negatively correlated with the clinical staging and the degree of basal cell liquefaction in OLP (clinical staging: r=-0.57, P=0.021; basal cell liquefaction: r=-0.54, P=0.032), but not with the disease duration and the degree of lymphocytic infiltration (P>0.05). Conclusions: Autophagy related factors LC3B, p62 and Beclin1 may play a role in the formation and progression of OLP lesions. The autophagy level was relatively lack in erosive OLP compared to non-erosive OLP, contributing to the increased local lesion destruction in erosive OLP. Abnormal cellular autophagy may play an important role in the formation of OLP lesions.
Humans ; Lichen Planus, Oral/metabolism* ; Beclin-1 ; Microtubule-Associated Proteins/metabolism* ; Autophagy ; RNA, Messenger/metabolism*

OBJECTIVETo investigate the role of microtubule-associated protein 2 (MAP-2) and nestin in gastric development in human embryos and fetuses.

METHODSImmunohistochemistry was used to detect the expressions of MAP-2 and nestin proteins in the gastric cardia, pyloric and gastric tissues of human embryos and fetuses during the second, third and fourth month of development.

RESULTSIn the second to fourth months of gestation, MAP-2 and nestin expressions were detected in the neural cells and neural fibers of the intermuscular nerve plexus and submucosal plexus in the gastric cardia, pyloric and gastric tissues. As the gestational age increased, the number of MAP-2- and nestin-positive cells and the expression intensity all increased in the myenteric plexus, but MAP-2 and nestin expressions were negative in the glandular and mucosal tissues of human embryonic and fetal gastric cardia, pylorus or gastric walls.

CONCLUSIONMAP-2 and nestin participate in the regulation of the development of gastric tissues in human embryos.

Fetus ; metabolism ; Humans ; Intermediate Filament Proteins ; metabolism ; Microtubule-Associated Proteins ; metabolism ; Nerve Tissue Proteins ; metabolism ; Nestin ; Stomach ; embryology ; metabolism

OBJECTIVETo explore the role of microtubule-associated protein 2 (MAP-2) and nestin in the development of tongue muscles of human embryos and fetuses.

METHODSPV immunohistochemistry was used to detect the expressions of MAP-2 and nestin proteins in the tongue tissues of human embryos and fetuses at the second, third and fourth months of gestation.

RESULTSMAP-2 and nestin positivity was detected in the tongue muscles of human embryos at 2 to 4 months of gestation. In the embryos at the second month of gestation, no obvious MAP-2 positive cells were found in the tongue muscles; at 3 and 4 months, the number of MAP-2-positive cells in the tongue muscles was 24.14∓8.28 and 15.86∓3.89, with the expression intensity of 109.42∓11.62 and 124.27∓8.73, respectively. At 2, 3 and 4 months of gestation, the number of nestin-positive cells in the tongue muscles was 12.50∓3.17, 19.00∓7.63, and 22.80∓6.91, with expression intensity of 119.99∓24.02, 102.20∓11.76, and 98.24∓10.66, respectively. As the gestational age increased, the number of MAP-2-positive cell number continued to decline following a transient increase but the expression intensity kept increasing; nestin-positive cells increased continuously but the expression intensity kept decreasing in the embryonic or fetal tongue muscles.

CONCLUSIONMAP-2 and nestin proteins are involved in the regulation of the development of tongue muscles in human embryos and fetuses.

Humans ; Microtubule-Associated Proteins ; metabolism ; Muscle, Skeletal ; embryology ; Nestin ; metabolism ; Tongue ; embryology

Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin's lymphoma (NHL), which is also a significantly heterogeneous disease. Survivin, a unique member of the inhibitor of apoptosis (IAP) family, is overexpressed in various cancers, including some types of lymphoma. It is found that inhibitor of apoptosis protein, survivin, plays an important role in the development and progression of DLBCL. Survivin is able to inhibit the cell apoptosis, and enhances the cell proliferation. Many studies showed that survivin may be considered as an independent unfavorable prognostic index of DLBCL. The poor prognostic cases early are screened in combination of survivin expression with International Prognostic Index (IPI), and improve the outcome of DLBCL. Survivin selectively expressed in tumor tissue, which provide an ideal target for tumor therapy. Modulation of survivin expression or function may provide a novel approach for experimental therapy in patients with DLBCL. In this review, the progress of study on mechanism of survivin protein, the survivin expression in DLBCL, its significance in diagnosis and therapy of DLBCL, and the prospective trend were summarized.
Apoptosis ; Humans ; Lymphoma, Large B-Cell, Diffuse ; metabolism ; pathology ; Microtubule-Associated Proteins ; biosynthesis

Asthenoteratozoospermia is one of the most severe types of qualitative sperm defects. Most cases are due to mutations in genes encoding the components of sperm flagella, which have an ultrastructure similar to that of motile cilia. Coiled-coil domain containing 103 (CCDC103) is an outer dynein arm assembly factor, and pathogenic variants of CCDC103 cause primary ciliary dyskinesia (PCD). However, whether CCDC103 pathogenic variants cause severe asthenoteratozoospermia has yet to be determined. Whole-exome sequencing (WES) was performed for two individuals with nonsyndromic asthenoteratozoospermia in a consanguineous family. A homozygous CCDC103 variant segregating recessively with an infertility phenotype was identified (ENST00000035776.2, c.461A>C, p.His154Pro). CCDC103 p.His154Pro was previously reported as a high prevalence mutation causing PCD, though the reproductive phenotype of these PCD individuals is unknown. Transmission electron microscopy (TEM) of affected individuals' spermatozoa showed that the mid-piece was severely damaged with disorganized dynein arms, similar to the abnormal ultrastructure of respiratory ciliary of PCD individuals with the same mutation. Thus, our findings expand the phenotype spectrum of CCDC103 p.His154Pro as a novel pathogenic gene for nonsyndromic asthenospermia.
Asthenozoospermia/pathology* ; Dyneins/genetics* ; Homozygote ; Humans ; Male ; Microtubule-Associated Proteins ; Mutation ; Mutation, Missense ; Sperm Tail/metabolism*

Humans ; Inhibitor of Apoptosis Proteins ; Microtubule-Associated Proteins ; genetics ; metabolism ; Protein Isoforms ; genetics ; metabolism ; Stomach Neoplasms ; genetics ; metabolism ; Tumor Cells, Cultured

OBJECTIVETo explore the expression of Survivin (SVV) protein in colorectal carcinogenesis and its clinical significance. METHODS Immunohistochemistry staining was performed by two-step EnVision technique for the paraffin sections, which included 90 adenomas, 25 ademomas with high-grade glandular intraepithelial neoplasia, and 108 colorectal adenocarcinomas.

RESULTSExpressions of SVV, P53, and Bcl-2 were observed in tumor cells of the sections. The positive rate of SVV in tubular adenomas, villous adenomas, and tubulovillous adenomas were 30% (12/40), 40.9% (9/22), and 35.8% (10/28), respectively. The positive rate of SVV in tubulovillous adenomas with high-grade glandular intraepithelial neoplasia were 68% (17/25). The positive rate of SVV in carcinomas of stage A, B, and C were 75% (27/36), 81.3% (26/ 32), and 95% (38/40), respectively. SVV expressions among the three types of adenomas without neoplasia were not significantly different (P > 0.05). SVV expression between each type of the above-mentioned ademoma and tubulovillous adenoma with high-grade glandular intraepithelial neoplasia or different Dukes stages of colorectal carcinoma was significantly different (P < 0.05). SVV expressions in adenocarcinomas and adenomas with high grade glandular intraepithelial neoplasia were significantly higher than those in adenomas (P < 0.01). The expressions of P53 and Bcl-2 had no significant difference among them. No association was noted between SVV expression and P53 or Bcl-2 expression (P = 0.487, P = 0. 437).

CONCLUSIONSSVV is abnormally expressed in the early stage of colorectal carcinogenesis, which may be correlated with the carcinogenesis of colorectal ademoma. SVV expression may be useful to distinguish adenocarcinoma from adenoma in colorectal carcinogenesis.

Adenocarcinoma ; metabolism ; pathology ; Adenoma ; metabolism ; pathology ; Colorectal Neoplasms ; metabolism ; pathology ; Humans ; Inhibitor of Apoptosis Proteins ; Microtubule-Associated Proteins ; biosynthesis

OBJECTIVETo develop the organophosphate-induced delayed neuropathy (OPIDN) hen model with 2,4,6-trimethylbenzoyl phenylphosphonate (TOCP), and observe the change of pathology and investigate the alterations of microtubulin associated protein 2 (MAP2).

METHODS48 adult hens were randomly divided into four groups, including three experimental groups and control group (n = 12 each group). The hens in three experimental groups were treated with TOCP by gavage at single dosages of 250, 500 and 750 mg/kg respectively while the control hens received an equivalent volume of corn oil by gavage. All hens were sacrificed after 21 days of treatment. Half hens in each group were dissected for HE examination and myelin straining of brain, spinal cord and sciatic nerve while brains of another half hens were dissected for the determination of MAP2 by western blotting.

RESULTSThe delayed neurotoxicity symptoms of hens both in 500 and 750 mg/kg groups were consistently observed. The pathological changes of brain, spinal cord and sciatic nerve in 500 and 750 mg/kg groups showed nerve cells difference necrosis, increased cytoplasm basophilia, microglia proliferation, mono-nuclear and lymphocyte infiltration, myelin sheath extensive up to part of them disaggregation deletion. Compared with the control group, at 500 and 750 mg/kg respectively the increase of MAP2 was 25% and 23% (P < 0.01 and P < 0.05).

CONCLUSIONSThe histopathologic changes of OPIDN caused by TOCP have dose-response relationship. The changes of MAP2 in nervous system may contribute to the occurrence and development of TOCP induced delayed neurotoxicity.

Animals ; Brain ; metabolism ; pathology ; Chickens ; Female ; Microtubule-Associated Proteins ; metabolism ; Nervous System Diseases ; chemically induced ; metabolism ; pathology ; Organophosphates ; toxicity