Journals / Journal of Mood Disorders / 2015 / Cilt: 5 - Sayı: 4

Increased High Mobility Group Box1 (HMGB1) level in major depressive disorder

Major Depresif Bozuklukta Artmış High Mobility Group Box1 (HMGB1) Düzeyi

Pages
145–150
Publication Date
2022-10-18
DOI
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⚡ TL;DR(Too Long; Didn't Read)

Results: Significantly higher HMGB1 values were identifiedwith the patient group when compared to the controlgroup (p

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: It was reported that High Mobility GroupBox 1 (HMGB1), also known as the nuclear transcriptionfactor, is a late mediator of inflammation.
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Key Findings & Data:It was thoughtthat HMGB1 has a prominent role in the activationof Tumor Necrosis Factor-α (TNF-α), Interleukin (IL)-1βand IL-8 which are proinflammatory mediators duringinflammation.
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Conclusion & Impact:Results: Significantly higher HMGB1 values were identifiedwith the patient group when compared to the controlgroup (p
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Objective: It was reported that High Mobility GroupBox 1 (HMGB1), also known as the nuclear transcriptionfactor, is a late mediator of inflammation. It was thoughtthat HMGB1 has a prominent role in the activationof Tumor Necrosis Factor-α (TNF-α), Interleukin (IL)-1βand IL-8 which are proinflammatory mediators duringinflammation. HMGB1 plays a role in progress, diagnosisand prognosis of immune system illnesses. Besidessuppressing the immune system, Major DepressiveDisorder (MDD) was indicated to cause changes ininflammatory processes. Biological determinants affectingthe diagnosis, therapy, and prognosis of depression arequite limited. Therefore, new etiological models areneeded to explain the pathophysiology of depression.There is no study in the literature investigating level ofHMGB1 in MDD of the humans. This study aims to examinethe role of inflammation in the etiology of depressionbased on the HMGB1 in patients with MDD.Methods: A total of 30 patients diagnosed with MDDwere included in the study. The control group consistedof 30 healthy subjects without any psychiatric disorders. Asocio-demographic information form, Hamilton DepressionRating Scale (HDRS) and Clinical Global Impression Scale(CGIS) were administered, and blood was taken formeasurement of HMGB1 levels. Results: Significantly higher HMGB1 values were identifiedwith the patient group when compared to the controlgroup (p

Özet

Amaç: Nükleer transkripsiyon faktörü olarak bilinen HighMobility Group Box1 (HMGB1)in inflamasyonun geç göstergesi olduğu bildirilmiştir. HMGB1in proinflamatuargöstergeler olan Tümör Nekroz Faktör-α (TNF-α), Interlökin(IL)-1β ve IL-8 aktivasyonunda önemli bir rolü olduğudüşünülmektedir. HMGB1 bağışıklık sistem hastalıklarınınseyrinde, teşhis ve hastalık prognozunun belirlenmesinderol oynamaktadır. Majör Depresif Bozukluğun (MDB) bağışıklık sistemi baskılamasının yanı sıra inflamatuar süreçlerde değişikliğe neden olduğu anlaşılmıştır. Depresyondatanı, tedavi ve prognozu etkileyen biyolojik belirleyicileroldukça sınırlıdır. Bu nedenle depresyon patofizyolojisiniaçıklamak için yeni etiyolojik modeller gerekmektedir.Literatürde insanlarda MDBde HMGB1 düzeyini inceleyençalışma bulunmamaktadır. Biz bu çalışmada MDB tanılıhastalarda HMGB1 düzeyini değerlendirerek inflamasyo- nun depresyon etiyolojisindeki yerini açıklamayı amaçladıkYöntem: Hasta grubu MDB tanılı 30 kişiden, kontrol grubuise herhangi bir psikiyatrik rahatsızlığı olmayan sağlıklı 30kişiden oluşmaktaydı. Katılımcılara bilgilendirilmiş gönüllüolur formu imzalatıldıktan sonra sosyodemografik bilgiformu ve Hamilton Depresyon Derecelendirme Ölçeği(HDDÖ), Klinik Global İzlem Ölçeği (KGİÖ) uygulandı.HMGB1 düzeyinin ölçümü için kan alındı. Bulgular: Hasta grubunun HMGB1 düzeyinin kontrol grubuna göre istatistiksel olarak anlamlı düzeyde yüksekolduğu görüldü (p

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Cite This Article

GÜNEŞ, M., OKAN, A. İ., KAYA, M. C., BULUT, M., ATLI, A., DEMİR, S., SEVİM, B., BEZ, Y., DEMİRPENÇE, Ö. (2022). Increased High Mobility Group Box1 (HMGB1) level in major depressive disorder. Journal of Mood Disorders, Cilt: 5 - Sayı: 4, 145–150. https://ajindex.com/articles/564584

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References (16)

  1. Zhang J, McCauley MJ, Maher LJ, Williams MC, Israeloff NE. Mechanism of DNA flexibility enhancement by HMGB proteins. Nucleic Acids Res. 2009;37:1107-14
  2. Kang HJ, Lee H, Choi HJ, Youn JH, Shin JS, Ahn YH, Yoo JS, Paik YK, Kim H. Non-histone nuclear factor HMGB1 is phosphorylated and secreted in colon cancers. Lab Invest. 2009;89:948-59
  3. Thomas JO, Travers AA. HMG1 and 2, and related ‘architectural’ DNA binding proteins. Trends Biochem Sci. 2001;26:167-74
  4. Muller S, Scaffidi P, Degryse B, Bonaldi T, Ronfani L, Agresti A, Beltrame M, Bianchi ME. New EMBO members’ review: the double life of HMGB1 chromatin protein: architectural factor and extracellular signal. Embo J. 2001;20:4337-40
  5. Todorova J, Pasheva E. High mobility group B1 protein interacts with its receptor RAGE in tumor cells but not in normal tissues. Oncol Lett. 2012;3:214-8
  6. Park JS, Arcaroli J, Yum HK, Yang H, Wang H, Yang KY, Choe KH, Strassheim D, Pitts TM, Tracey KJ, Abraham E. Activation of gene expression in neutrophils by high mobility group box 1 protein. Am J Physiol Cell Physiol. 2003;284:870-9
  7. Tian J, Avalos AM, Mao SY, Chen B, Senthil K, Wu H, et al. Toll- like receptor 9-dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE. Nat Immunol. 2007;8:487-96
  8. Degryse B, de Virgilio M. The nuclear protein HMGB1, a new kind of chemokine. FEBS Lett. 2003;553:11-7
  9. Moriwaka Y, Luo Y, Ohmori H, Fujii K, Tatsumoto N, Sasahira T, et al. HMGB1 attenuates anti-metastatic defense of the lymph nodes in colorectal cancer. Pathobiology. 2010;77:17-23
  10. Bianchi ME. HMGB1 loves company. J Leukocyte Biol. 2009;86:573-6
  11. Tuğlu C, Kara SH. Depresyon, sitokinler ve bağışıklık sistemi. Klinik Psikofarmakoloji Bülteni. 2003;13:142-150
  12. Raison CL, Capuron L, Miller AH. Cytokines sing the blues: inflammation and the pathogenesis of depression. Trends Immunol. 2006;27:24-31
  13. Janssen DG, Caniato RN, Verster JC, Baune BT. A psychoneuroimmunological review on cytokines involved in antidepressant treatment response. Hum Psychopharmacol. 2010;25:201-15
  14. Krishnadas R, Cavanagh J. Depression: an inflammatory illness? J Neurol Neurosurg Psychiatry. 2012; 83:495-502
  15. Sankowski R, Mader S, Ferrer SIV. Systemic inflammation and the brain: novel roles of genetic, molecular, and environmental cues as drivers of neurodegeneration. Front Cell Neurosci. 2015;9:1-20
  16. Terrando N, Rei Fidalgo A, Vizcaychipi M, Cibelli M, Ma D, Monaco C, et al. Th