Role of microrna-199 in nsc-34 cell model for treatment ofamyotrophic lateral sclerosis
Başlık çevirisi mevcut değil.
- Tez No: 772154
- Danışmanlar: DR. KATARZYNA WHYSALL
- Tez Türü: Yüksek Lisans
- Konular: Mikrobiyoloji, Microbiology
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 2022
- Dil: İngilizce
- Üniversite: Università degli Studi di Torino
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 41
Özet
Neurodegenerative diseases are important research area because their progressive phase cause motor muscle and neurons dysfunctions, neuronal disconnections, muscle weakness, and death. All over the world, many laboratories and research groups work on neurodegenerative disease to understand mechanisms and enhance possible treatment. Amyotrophic lateral sclerosis (ALS) is highly aggressively progressive neurodegenerative diseases which characterized cell death of motor neurons in brain and spinal cord. With aging, neuron cells increase and become aggressive state. There are familial and sporadic type ALS which are based on genetic inheritance or mutation cause. For neurodegenerative diseases still there is no drugs or treatments. Understanding for ALS mechanism is essential to understand neuron stem cells differentiation, proliferation, signaling pathways, systematic responses, miRNA responses and characterizations. In this master thesis, we used NSC-34 cell line that is murine neuroblastoma/spinal cord hybrid cell line produced by fusion of mouse neuroblastoma cells with motoneuron-enriched embryonic spinal cord cells. NSC-34 cells show similar features with mature primary motor neurons. Because of these features of NSC-34 cell line, it is an established in vitro model to study neuronal development, differentiation, and oxidative stress. It is deemed appropriate to study neurodegeneration, such as during ALS. In literature, many different differentiation and proliferation mediums found. However, possible miRNA treatment of ALS, we need both proliferation and differentiation together. For NSC-34 cells differentiation, 1%FBS, DMEM: F12, Horse serum and retinoic acid mediums compared. miR-199 and muscle relation showed in previous article and miR-199 has regenerative effect on ALS mice' muscle and NMJ properties. However, for neuron relation wasn't investigated. To investigate miR-199 role in neurodegeneration, we treated NSC-34 cells with miR-199 and antagomir miRNA-199 (AmiR199). Neuron length compared each other to underline neuronal differentiation. In this study we showed that differentiation of NSC-34 cell maximized with DMEM: F12 medium compared to 1%FBS, Horse serum and retinoic acid mediums. In the presence RA, exhibited higher concentration of 0.5 uM retinoic acid is toxic for NSC-34 cells and 20x103 cells/per well showed higher differentiation result. miR-199 treatment on NSC-34 cells results present that miR199 induced differentiation and proliferation. Highest average neuron length is miR-199 treatment which is dominant form for neurons. Antagomir miRNA-199 has lower average neuron length than miR-199 but higher than scramble miRNAs. According to this result we can conclude that miR-199 boost factor for neuron differentiation. NSC-34 cell line differentiation, proliferation and miR-199 studies proved that miRNA-199 has high potential for neuron studies. So, by taking muscle regeneration results in previous studies and neuron differentiation results in my thesis into account, miR-199 might be key factor for further ALS studies.
Özet (Çeviri)
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