scholarly journals Intraperitoneal administration of activin A promotes development of endometriotic lesions in a mouse model of endometriosis

2019 ◽  
Vol 66 (1.2) ◽  
pp. 123-127 ◽  
Author(s):  
Kana Kasai ◽  
Takeshi Kato ◽  
Yuri Kadota ◽  
Otgontsetseg Erdenebayar ◽  
Kaoru Keyama ◽  
...  
Keyword(s):  
Mouse Model ◽  
Intraperitoneal Administration ◽  
Activin A

An Acvr1[R258G] ‘conditional on' mouse model of atypical fibrodysplasia ossificans progressiva (FOP) is Activin A dependent

2019 ◽  
Author(s):  
Lily Huang ◽  
Chris Schoenherr ◽  
Lili Wang ◽  
Xialing Wen ◽  
Joyce McClain ◽  
...  
Keyword(s):  
Mouse Model ◽  
Activin A ◽  
Fibrodysplasia Ossificans Progressiva

scholarly journals Identifying a New Mechanism of Sarcopenia by Autophagy

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A50-A50
Author(s):  
Eijiro Yamada ◽  
Ryota Uehara ◽  
Yasuyo Nakajima ◽  
Kazuhiko Horiguchi ◽  
Emi Ishida ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Mouse Model ◽  
Hind Limb ◽  
Tibialis Anterior Muscle ◽  
Intraperitoneal Administration ◽  
Gene Expressions ◽  
The Metabolic Syndrome ◽  
Hind Limb Suspension ◽  
Stat3 Phosphorylation ◽  
Autophagy Activity

Abstract Sarcopenia is one of the critical factors in reducing Activity of Daily Life and associated with morbidity and mortality. Sarcopenia has also been linked to metabolic syndrome. In recent years, it has been reported that autophagy is one of the mechanisms as a cause of sarcopenia. Therefore, we focused on autophagy as a system that can regulate both sarcopenia and metabolic syndrome in skeletal muscle and revealed that non-receptor tyrosine kinase Fyn not only participates in metabolic syndrome but also regulates autophagy regulating sarcopenia through STAT3 regulation, mainly using transgenic mice (Cell metabolism 2010, Cell Rep. 2012). However, since these were non-physiological studies, we proceeded with further studies and demonstrating that Fyn dependent STAT3 phosphorylation by IL6, which is involved in chronic inflammation and metabolic syndrome, was observed in mouse C2C12 myotube cells. Autophagy was decreased in those cells by both IL6 dependent and Fyn dependent mechanisms. Furthermore, in the denervated mouse model, not only both Fyn and IL6 gene expressions as well as the key muscle specific E3 ubiquitin ligases, Atrogin1 and MuRf1 were increased but the expression and phosphorylation levels of STAT3 were also augmented, while the autophagy activity was decreased. We believe that a denervated mouse model alone is not enough as a model for sarcopenia, thus we next introduced a hind limb suspension mouse model that promotes disuse atrophy by suspending the hind limb. Using this model, we found that muscle atrophy was observed mainly in the soleus muscle, tibialis anterior muscle, and the gastrocnemius muscle with Atrogin1 and MuRf1 increased. Increase of both IL6 and STAT3 expression/phosphorylation were also observed in the muscles of hind limb suspension mice. Autophagy activity, examined by intraperitoneal administration of colchicine, was decreased. These results strongly suggest that Fyn is involved not only in the metabolic syndrome but also in the pathogenesis of sarcopenia, and may lead to a better understanding of the pathology of sarcopenia obesity and the development of therapeutic methods.

scholarly journals Activin A Is Anti-Lymphangiogenic in a Melanoma Mouse Model

2015 ◽  
Vol 135 (1) ◽  
pp. 212-221 ◽  
Author(s):  
Magdalena Heinz ◽  
Heide Leb Niederleithner ◽  
Emmi Puujalka ◽  
Ana Soler-Cardona ◽  
Michael Grusch ◽  
...  
Keyword(s):  
Mouse Model ◽  
Activin A

Inhibition of activin A signalling in a mouse model of pre-eclampsia

Placenta ◽  
2015 ◽  
Vol 36 (8) ◽  
pp. 926-931 ◽  
Author(s):  
R. Lim ◽  
S. Adhikari ◽  
S. Gurusinghe ◽  
B. Leaw ◽  
R. Acharya ◽  
...  
Keyword(s):  
Mouse Model ◽  
Activin A

scholarly journals Involvement of infiltrating macrophage-derived activin A in the progression of renal damage in MRL-lpr mice

2017 ◽  
Vol 312 (2) ◽  
pp. F297-F304 ◽  
Author(s):  
Anastasie Tshilela Kadiombo ◽  
Akito Maeshima ◽  
Ken Kayakabe ◽  
Hidekazu Ikeuchi ◽  
Toru Sakairi ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Lupus Erythematosus ◽  
Renal Damage ◽  
Transforming Growth Factor ◽  
Intraperitoneal Administration ◽  
Transforming Growth Factor Β ◽  
Activin A ◽  
Dependent Manner ◽  
Cytokines And Chemokines

Lupus nephritis is a life-threatening complication of systemic lupus erythematosus (SLE). Various growth factors, cytokines, and chemokines are implicated in the development of SLE. However, the pathophysiological processes involved in the development of lupus nephritis still remain unclear. In this study, we examined the involvement of activin A, a member of the transforming growth factor β (TGF-β) superfamily, in the progression of renal damage in lupus-prone MRL- lpr mice. Activin A was not expressed in the kidneys of control MRL-MpJ mice but was detectable in perivascular infiltrating cluster of differentiation 68 (CD68)-positive cells in the kidneys of MRL- lpr mice. Urinary activin A, which was also absent in MRL-MpJ mice, was detectable in MRL- lpr mice from 16 wk onward. Urinary activin A levels were significantly correlated with the number of perivascular inflammatory cell layers, the number of crescentic glomeruli, and the percentage of Elastica van Gieson (EVG)-positive fibrotic areas, but not with urinary protein levels or serum activin A. When activin action was blocked in vivo by the intraperitoneal administration of an activin antagonist, follistatin, the number of crescentic glomeruli, percentage of EVG-positive fibrotic areas, CD68-positive cell infiltration, and proteinuria were significantly reduced in a dose-dependent manner. These data suggest that infiltrating macrophage-derived activin A is involved in the progression of renal damage in MRL- lpr mice.

scholarly journals Cross-Reactivity against Naja sumatrana (Black Spitting Cobra) Envenoming from the Haffkine Antivenom in a Mouse Model

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Gregory Cham ◽  
Francis Lim ◽  
Arul Earnest ◽  
Ponnampalam Gopalakrishnakone
Keyword(s):  
Mouse Model ◽  
Standard Error ◽  
Challenge Test ◽  
Intraperitoneal Administration ◽  
Cross Reactivity ◽  
Naja Naja ◽  
Swiss Albino Mice ◽  
Tail Vein ◽  
Albino Mice

Naja sumatrana is the dominant cobra species in Malaysia, Singapore, Borneo, and Sumatra, and it does not have specific antivenom. The Haffkine antivenom has been advocated instead. This study aims to determine the efficacy of this antivenom against Naja sumatrana envenoming using a mouse model. Methods. Male Swiss albino mice were used. Intravenous LD50 was first determined separately for Naja naja and Naja sumatrana venom. ED50 was determined by preincubating antivenom with each venom at 2.5 LD50 before administering the mixture into the tail vein. Validation was carried out using a challenge test. Each mouse received 111 µg of Naja sumatrana venom intramuscularly followed by intraperitoneal administration of dilute Haffkine antivenom. Survival was recorded 24 hours after envenoming. Results. The LD50 of Naja naja venom was 78.13 µg, standard error (SE) 13.3 µg. The ED50 of the Haffkine antivenom against Naja naja venom was 45.9 mg, SE 7.5 mg. The LD50 and ED50 of Naja sumatrana venom were 55.5 µg, SE 12.0 µg; and 73.9 mg, SE 12.0 mg, respectively. The intra-peritoneal ED50 against 111 µg intramuscular Naja sumatrana venom was 136.95 mg, SE 36.74 mg. Conclusion. The Haffkine polyvalent antivenom exhibited cross-neutralisation against Naja sumatrana venom when used at a higher dose.

scholarly journals Intraperitoneal Administration of Synthetic MicroRNA-214 Exhibits Tumor Suppression in an Intraperitoneal Dissemination Mouse Model of Canine Hemangiosarcoma

2021 ◽  
Author(s):  
Ryutaro Yoshikawa ◽  
Atsushi Maeda ◽  
Yoshihito Ueno ◽  
Hiroki Sakai ◽  
Shintaro Kimura ◽  
...  
Keyword(s):  
Mouse Model ◽  
Caspase 3 ◽  
Systemic Treatment ◽  
Chemotherapeutic Agent ◽  
Intraperitoneal Administration ◽  
Median Number ◽  
Antitumor Effects ◽  
Ki 67 ◽  
Novel Mirna ◽  
Nuclease Resistance

Abstract Canine hemangiosarcoma (HSA) has extremely poor prognosis, making it necessary to develop new systemic treatment methods. MicroRNA-214 (miR-214) is one of many microRNAs (miRNA) that can induce apoptosis in HSA cell lines. Synthetic miR-214 (miR-214/5AE), which showed higher cytotoxicity and greater nuclease resistance than mature miR-214, has been developed for clinical application. In this study, we evaluated the effects of miR-214/5AE on stage 2 HSA in a mouse model. Mice intraperitoneally administered with miR-214/5AE (5AE group) had significantly fewer intraperitoneal dissemination tumor foci (median number: 80 vs. 233; p < 0.05) and lighter median foci weight (0.26 g vs. 0.74 g; p < 0.05). There was an increase in p53 and cleaved caspase-3 expression in the 5AE group. The mice in this group also had a significantly lower proportion of Ki-67-positive cells than those in the non-specific miR group. Notably, there were no significant side effects observed. These results indicate that intraperitoneal administration of miR-214/5AE exhibits antitumor effects in the intraperitoneal dissemination mouse model of HSA by inducing apoptosis and suppressing cell proliferation. We strongly believe that miR-214/5AE could be a novel miRNA-based chemotherapeutic agent capable of improving the prognosis of HSA.

scholarly journals Neuroprotective Effects of Tripeptides—Epigenetic Regulators in Mouse Model of Alzheimer’s Disease

2021 ◽  
Vol 14 (6) ◽  
pp. 515
Author(s):  
Vladimir Khavinson ◽  
Anastasiia Ilina ◽  
Nina Kraskovskaya ◽  
Natalia Linkova ◽  
Nina Kolchina ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Dna Sequences ◽  
Dendritic Spine ◽  
Molecular Mechanisms ◽  
Neuroprotective Effect ◽  
Intraperitoneal Administration ◽  
Neuroprotective Effects ◽  
Model Of Alzheimer’S Disease

KED and EDR peptides prevent dendritic spines loss in amyloid synaptotoxicity in in vitro model of Alzheimer’s disease (AD). The objective of this paper was to study epigenetic mechanisms of EDR and KED peptides’ neuroprotective effects on neuroplasticity and dendritic spine morphology in an AD mouse model. Daily intraperitoneal administration of the KED peptide in 5xFAD mice from 2 to 4 months of age at a concentration of 400 μg/kg tended to increase neuroplasticity. KED and EDR peptides prevented dendritic spine loss in 5xFAD-M mice. Their action’s possible molecular mechanisms were investigated by molecular modeling and docking of peptides in dsDNA, containing all possible combinations of hexanucleotide sequences. Similar DNA sequences were found in the lowest-energy complexes of the studied peptides with DNA in the classical B-form. EDR peptide has binding sites in the promoter region of CASP3, NES, GAP43, APOE, SOD2, PPARA, PPARG, GDX1 genes. Protein products of these genes are involved in AD pathogenesis. The neuroprotective effect of EDR and KED peptides in AD can be defined by their ability to prevent dendritic spine elimination and neuroplasticity impairments at the molecular epigenetic level.

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