• 제목/요약/키워드: Smooth muscle cell

검색결과 398건 처리시간 0.025초

The Pathophysiologic Roles of TRPM7 Channel

  • Park, Hyun Soo;Hong, Chansik;Kim, Byung Joo;So, Insuk
    • The Korean Journal of Physiology and Pharmacology
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    • 제18권1호
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    • pp.15-23
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    • 2014
  • Transient receptor potential melastatin 7 (TRPM7) is a member of the melastatin-related subfamily and contains a channel and a kinase domain. TRPM7 is known to be associated with cell proliferation, survival, and development. It is ubiquitously expressed, highly permeable to $Mg^{2+}$ and $Ca^{2+}$, and its channel activity is negatively regulated by free $Mg^{2+}$ and Mg-complexed nucleotides. Recent studies have investigated the relationships between TRPM7 and a number of diseases. TRPM7 regulates cell proliferation in several cancers, and is associated with ischemic cell death and vascular smooth muscle cell (VSMC) function. This review discusses the physiologic and pathophysiologic functions and significance of TRPM7 in several diseases.

Decreased inward rectifier and voltage-gated K+ currents of the right septal coronary artery smooth muscle cells in pulmonary arterial hypertensive rats

  • Kim, Sung Eun;Yin, Ming Zhe;Kim, Hae Jin;Vorn, Rany;Yoo, Hae Young;Kim, Sung Joon
    • The Korean Journal of Physiology and Pharmacology
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    • 제24권1호
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    • pp.111-119
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    • 2020
  • In vascular smooth muscle, K+ channels, such as voltage-gated K+ channels (Kv), inward-rectifier K+ channels (Kir), and big-conductance Ca2+-activated K+ channels (BKCa), establish a hyperpolarized membrane potential and counterbalance the depolarizing vasoactive stimuli. Additionally, Kir mediates endothelium-dependent hyperpolarization and the active hyperemia response in various vessels, including the coronary artery. Pulmonary arterial hypertension (PAH) induces right ventricular hypertrophy (RVH), thereby elevating the risk of ischemia and right heart failure. Here, using the whole-cell patch-clamp technique, we compared Kv and Kir current densities (IKv and IKir) in the left (LCSMCs), right (RCSMCs), and septal branches of coronary smooth muscle cells (SCSMCs) from control and monocrotaline (MCT)-induced PAH rats exhibiting RVH. In control rats, (1) IKv was larger in RCSMCs than that in SCSMCs and LCSMCs, (2) IKv inactivation occurred at more negative voltages in SCSMCs than those in RCSMCs and LCSMCs, (3) IKir was smaller in SCSMCs than that in RCSMCs and LCSMCs, and (4) IBKCa did not differ between branches. Moreover, in PAH rats, IKir and IKv decreased in SCSMCs, but not in RCSMCs or LCSMCs, and IBKCa did not change in any of the branches. These results demonstrated that SCSMC-specific decreases in IKv and IKir occur in an MCT-induced PAH model, thereby offering insights into the potential pathophysiological implications of coronary blood flow regulation in right heart disease. Furthermore, the relatively smaller IKir in SCSMCs suggested a less effective vasodilatory response in the septal region to the moderate increase in extracellular K+ concentration under increased activity of the myocardium.

혈관평활근세포에서 HSP90에 의한 IL-6 발현에 TLR-4와 NF-κB의 작용 (Roles of TLR-4 and NF-κB in Interleukin-6 Expression Induced by Heat Shock Protein 90 in Vascular Smooth Muscle Cells)

  • 임병용;김강성;김관회
    • 생명과학회지
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    • 제18권12호
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    • pp.1637-1643
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    • 2008
  • HSP90에 노출된 혈관평활근세포에서 IL-6 transcript가 증가하고, IL-6 단백질의 분비가 증가하며, 또한 IL-6 유전자의 promote가 활성화되었다. HSP90에 의한 IL-6 유전자의 promoter 활성화는 dominant negative 형태의 TLR-4와 MyD88에 의하여 크게 감소되었지만, dominant negative 형태의 TLR-3와 TRIF의 영향을 받지 않았다. 그리고 TLR-4의 이합체화(dimerization)를 저해하는 curcumin은 HSP90에 의한 IL-6의 분비 및 IL-6 유전자 promoter 활성화를 억제하였다. 그리고 IL-6 유전자의 promoter의 NF-${\kappa}B$- 또는 C/EBP-binding sequence에 변이는 HSP90에 의한 IL-6 유전자의 promoter 활성화 억제하였다. 이러한 결과는 혈관평활근세포에서 HSP90에 의한 IL-6 유전자 활성화에 TLR-4와 NF-${\kappa}B$B가 관여함을 의미한다.

가미통규탕(加味通竅湯)이 호흡기 뮤신 분비 및 기관 평활근 긴장도에 미치는 영향 (Effect of Gamitonggyu-tang on Secretion of Airway Mucin and Contractility of Tracheal Smooth Muscle)

  • 이남열;한재경;김윤희
    • 대한한방소아과학회지
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    • 제21권3호
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    • pp.109-124
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    • 2007
  • Objectives In the present study, the author intended to investigate whether Gamitonggyu-tang (GTT) significantly affects (since the subject is GTT, you need an 's') in vivo and in vitro mucin secretion from airway epithelial cells. Methods In vivo experiment, mice's mucin which is on a hypersecretion of an airway, mice's tracheal goblet cells in hyperplasia and mice's intraepithelial mucosubstances were exposed with SO2 for 3 weeks. Effects of orally-administered GTT for 1 week on in vivo mucin secretion and hyperplasia of tracheal goblet cells were assessed by using enzyme-linked immunosorbent assay (ELISA) and staining goblet cells with alcian blue. In vitro experiment, confluent hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled with 3H-glucosamine for 24 hrs and chased for 30 min in the presence of GTT to figure out the effectiveness of 3H-mucin secretion. Total elution profiles of control spent media and treatment sample through Sepharose CL-4B column were analyzed.Possible cytotoxicities of each agent were assessed by measuring lactate dehydrogenase (LDH) release. Also, the effect of GTT on contractility of isolated tracheal smooth muscle was investigated. Results (1) GTT inhibited hypersecretion of in vivo mucin. However, it did not affect the increase the number of goblet cells (2) GTT significantly increased mucin release from cultured HTSE cells, without significant cytotoxicity (3) GTT chiefly affected the 'mucin' secretion and did not affect the secretion of the other releasable glycoproteins with less molecular weight than mucin (4) GTT did not affect Ach-induced contraction of isolated tracheal smooth muscle.Conclusions This result suggests that GTT can increase mucin secretion during short-term treatment (in vitro) whereas it can inihibit hypersecretion of mucin during long-term treatment (in vivo). The author suggests that the effect GTT with their components should be further investigated and it is valuable to find from oriental medical prescriptions, novel agents which might regulate mucin secretion from airway epithelial cells.

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Intracellular pH regulation of mesenterffic arteriolar smooth myocytes of rat

  • Cho, Hyun-Sook;Park, Ki-Rang;Jang, Yeon-Jin;Park, Chun-Sik;Lee, Chae-Hun m
    • 한국생물물리학회:학술대회논문집
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    • 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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    • pp.57-57
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    • 2001
  • Intracellular pH(pH$\sub$i/) is strictly regulated since it is related to various cellular events such as contractility, signal transduction, ion regulation, cell volume, and energy production etc. In physiological conditions, pH$\sub$i/ of arteriolar smooth muscle faced substantial pressure to be changed during the regulation of blood flow. Therefore it is very important to know the regulatory mechanism of pH$\sub$i/.(omitted)

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쥐 상장간막 동맥과 그 분지에서 pH 변화가 혈관평활근 수축성에 미치는 영향 (Effect of pH Change on Vascular Smooth Muscle Contractility in Rat Superior Mesenteric Artery and Its Branches)

  • 최수승
    • Journal of Chest Surgery
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    • 제43권4호
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    • pp.345-355
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    • 2010
  • 산성화를 초래하는 Hypoxia 등 여러 가지 조건에서 변화하는 세포외 pH 변화는 궁극적으로 세포내 pH 변화를 유발하며 세포 내외 pH 변화는 혈관평활근 수축성 변화를 유발한다. 이러한 세포 내외 pH 변화에 의한 혈관 수축성 변화 기전을 규명하고자, pH 변화가 혈관수축인자들에 의한 혈관평활근 수축, 혈관평활근세포내 $Ca^{2+}$ 농도, 그리고 혈관평활근의 $Ca^{2+}$에 대한 민감도에 미치는 영향을 알아보고자 하였다. 대상 및 방법: 쥐에서 분리한 상장간막동맥과 그 분지에서 등장성 수축을 기록하였으며 배양한 상장간막동맥 세포에서 세포내 $Ca^{2+}$ 변화를 측정하였다. 세포외 pH는 정상인 7.4에서 6.4, 6.9 혹은 7.8로 변화시켰으며, 세포내 pH 변화는 propionic acid나 $NH_4$를 투여하거나 ${\beta}$-escin으로 세포막의 투과성을 증가시켜 세포외 용액의 pH 변화로 유발시켰다. 결과: 세포외 pH를 7.4에서 6.9, 6.4로 감소시키면 노에피네프린과 세로토닌에 의한 용량-반응 곡선이 우측 이동하였으며 최대 수축력의 50% 수축력을 유발하는 농도(half maximal effective concentration)가 증가하였고, pH를 7.8로 증가시키면 그 반대 현상이 일어났다. 노에피네프린은 배양한 혈관평활근세포에서 세포내 $Ca^{2+}$ 농도를 증가시켰으며, 이 세포내 $Ca^{2+}$ 증가는 세포외 pH 감소에 의하여 억제되었으며 세포외 pH 증가에 의하여 증가하였다. 노에피네프린에 의한 수축은 세포내 pH를 감소시키는 $NH_4$에 의하여 억제된 반면, 안정 장력은 $NH_4$과 propionic acid에 의하여 증가하였다. ${\beta}$-escin으로 세포막의 투과도를 증가시킨 후 세포외 용액의 $Ca^{2+}$ 농도를 증가시켜 수축을 유발시킨 후 세포외 용액의 pH를 변화시키면 pH 감소에 의하여 수축력이 감소하였으며 증가에 의하여 수축력이 증가하였다. 결론: 세포외 pH의 감소는 혈관평활근의 수축성을 감소시키는데 이는 세포외 pH 감소에 의한 혈관평활근의 혈관수축물질에 대한 반응성 감소, 혈관평활근 세포내 $Ca^{2+}$ 유입 억제 그리고 $Ca^{2+}$에 대한 혈관평활근의 민감성 감소에 의하여 일어난 것으로 추정할 수 있었다.

흉쇄유돌근에서 기인한 Low-Grade Myofibroblastic Sarcoma 1예 (Low Grade Myofibroblastic Sarcoma of the Sternocleidomastoid Muscle)

  • 심남석;홍현준;송기재;최성은;서연석;이은정
    • 대한두경부종양학회지
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    • 제30권1호
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    • pp.23-27
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    • 2014
  • Low-grade myofibroblastic sarcoma is a rare disorder of malignant soft tissue tumor and is usually occurred various regions that often manifests in the head and neck region. The most common clinical presentation of this entity is non-tender cervical lymphadenopathy. This disease usually presents high possibility of local recurrence and low possibility of distant metastasis. We report a rare case of low-grade myofibroblastic sarcoma occurring in the sternocleidomastoid muscle and invading to the mastoid tip. A 56-year-old male visited the clinic with a complaint of slowly growing postauricular mass for 6 months. Mass originating from sternomastoid muscle and invasion to mastoid tip was observed by imaging studies. Surgical complete excision with simple mastoidectomy was performed via modified facelift approach. The histopathologic findings revealed malignant spindle cell tumor with positive staining with smooth muscle actin. The patient has no recurrence for 2years without any complication.

Hyposmotic Cell Stretch Increases L-type Calcium Current in Smooth Muscle Cells of the Human Stomach

  • Kang, Tong-Mook;Kim, Chun-Hee;Kim, Min-Jung;Park, Myoung-Kyu;Uhm, Dae-Yong;Rhee, Jong-Chul;Rhee, Poong-Lyul
    • 한국생물물리학회:학술대회논문집
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    • 한국생물물리학회 1998년도 학술발표회
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    • pp.39-39
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    • 1998
  • Stretch-activated ion channel that is open by mechanical stress applied on the cell membrane is one of the classes of ion channels. Other than stretch-activated channel itself, it has been also reported that a variety of ion channels could be modulated by a mechanical cell stretch.(omitted)

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정맥기형 환자에 있어서의 유전자 발현 차이 (Difference of Gene Expression in Venous Malformation)

  • 김택균;오은정;조병채;정호윤
    • Archives of Plastic Surgery
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    • 제34권6호
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    • pp.671-678
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    • 2007
  • Purpose: Venous malformation(VM) which often causes pain and discomfort is the most common type of vascular malformations. Although it is presented with disfigured appearance and associated soft tissue or skeletal hypertrophy, the molecular bases of VMs are poorly understood. Differentially expressed genes(DEGs) of VMs were investigated to illuminate the molecular mechanism of the disease entity. Methods: Gene expressions of VM patients' subcutaneous tissue were studied in comparison with normal persons' by $GeneFishing^{TM}$ technique using the annealing control primers (ACPs) to identify DEGs. Candidate genes were sequenced and screened by basic local alignment search tool (BLAST) afterwards. Results: Among seventy DEGs identified, forty DEGs which had shown significantly different expression pattern were sequenced. Twenty eight out of 40 were up-regulated while 12 were down-regulated. BLAST searches revealed that 37 were known genes and 3 were unknown genes. Many genes were involved in the differentiation and remodeling of smooth muscle cells, opposed to the previous hypothesis that a lot of angiogenetic genes would be involved. Furthermore, several transcription factors and related genes, as well as cell signaling and metabolism regulators, were up regulated. Conclusion: It suggests that analysis of DEGs in VMs provide basic knowledge about its pathophysiology. and new therapeutic approaches.