{"id":{"repo_id":"ajou","oai_identifier":"oai:repository.ajou.ac.kr:201003/1295"},"canonical_url":"https://search.dev.ndltd.org/etd/ajou/oai:repository.ajou.ac.kr:201003/1295","repository":{"repo_id":"ajou","name":"Ajou University","base_url":"http://repository.ajou.ac.kr/oai/request"},"display":{"title":"Role of Extracellular Signal­-Regulated Kinase and Peroxisome Proliferator-­Activated Receptor gamma on Transforming Growth Factor-­β1-­Induced Human Endometrial Stromal Cell Decidualization","abstract":"OBJECTIVE: To investigate the role of ERK and PPAR gamma on TGF-β1-induced human endometrial stromal cell decidualization in vitro. MATERIALS AND METHODS: Human endometrial tissues obtained by hysterectomy specimens from patients with conditions other than endometrial diseases such as leiomyoma. Endometrial stromal cells were cultured under the following conditions: DMEM/F-12 (10% FBS, 1 nM E2 and 100 nM P4). 5 ng/ml of TGF-β1, 50 nM of rosiglitazone (PPAR gamma agonist), and 20 μM of PD98059 (ERK inhibitor) were added according to experimental purposes. Trypan-blue and a hemocytometer were utilized to count the viable cell number. Enzyme-linked immunosorbent assay (ELISA) and Western blotting was employed to detect proteins. RESULTS: TGF-β1 inhibited proliferation of cultured human endometrial stromal cells and induced expression of prostaglandin E2 (PGE2) and prolactin. This effect was mediated by Smad and ERK activation. Addition of rosiglitazone, a PPAR gamma agonist, prevented TGF-β1 effect on endometrial cell proliferation. Furthermore, rosiglitazone inhibited TGF-β1 induced activation of ERK, consequently reducing PGE2 and prolactin production. CONCLUSION: TGF-β1-induced decidualization of endometrial stromal cells through Smad and ERK phosphorylation. PPAR gamma acts as a negative regulator of human endometrial cell decidualization in vitro.","abstract_html":"OBJECTIVE: To investigate the role of ERK and PPAR gamma on TGF-β1-induced human endometrial stromal cell decidualization in vitro. MATERIALS AND METHODS: Human endometrial tissues obtained by hysterectomy specimens from patients with conditions other than endometrial diseases such as leiomyoma. Endometrial stromal cells were cultured under the following conditions: DMEM/F-12 (10% FBS, 1 nM E2 and 100 nM P4). 5 ng/ml of TGF-β1, 50 nM of rosiglitazone (PPAR gamma agonist), and 20 μM of PD98059 (ERK inhibitor) were added according to experimental purposes. Trypan-blue and a hemocytometer were utilized to count the viable cell number. Enzyme-linked immunosorbent assay (ELISA) and Western blotting was employed to detect proteins. RESULTS: TGF-β1 inhibited proliferation of cultured human endometrial stromal cells and induced expression of prostaglandin E2 (PGE2) and prolactin. This effect was mediated by Smad and ERK activation. Addition of rosiglitazone, a PPAR gamma agonist, prevented TGF-β1 effect on endometrial cell proliferation. Furthermore, rosiglitazone inhibited TGF-β1 induced activation of ERK, consequently reducing PGE2 and prolactin production. CONCLUSION: TGF-β1-induced decidualization of endometrial stromal cells through Smad and ERK phosphorylation. PPAR gamma acts as a negative regulator of human endometrial cell decidualization in vitro.","abstract_has_math":false,"creators":["장, 혜진"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["황, 경주","대학원 의학과","103765"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-01-26T05:22:12Z","date_published":"2011-01-26T05:22:12Z","updated_at":"2026-07-24T00:51:19Z","subjects":["Decidualization","TGF-β1","PPAR gamma","자궁내막","탈락막화"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000002027","000000002027"],"render_values":[{"text":"http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000002027","href":"http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000002027","code":true},{"text":"000000002027","href":null,"code":true}]}]},"links":{"outbound_url":"http://repository.ajou.ac.kr/handle/201003/1295","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["황, 경주","대학원 의학과","103765","장, 혜진"]},{"key":"dc:creator","label":"Author","values":["장, 혜진"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2011-01-26T05:22:12Z","2007"]},{"key":"dc:type","label":"Dc Type","values":["Thesis","Theses"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Decidualization","TGF-β1","PPAR gamma","자궁내막","탈락막화"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://repository.ajou.ac.kr/handle/201003/1295","http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000002027","000000002027"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["OBJECTIVE: To investigate the role of ERK and PPAR gamma on TGF-β1-induced human endometrial stromal cell decidualization in vitro. MATERIALS AND METHODS: Human endometrial tissues obtained by hysterectomy specimens from patients with conditions other than endometrial diseases such as leiomyoma. Endometrial stromal cells were cultured under the following conditions: DMEM/F-12 (10% FBS, 1 nM E2 and 100 nM P4). 5 ng/ml of TGF-β1, 50 nM of rosiglitazone (PPAR gamma agonist), and 20 μM of PD98059 (ERK inhibitor) were added according to experimental purposes. Trypan-blue and a hemocytometer were utilized to count the viable cell number. Enzyme-linked immunosorbent assay (ELISA) and Western blotting was employed to detect proteins. RESULTS: TGF-β1 inhibited proliferation of cultured human endometrial stromal cells and induced expression of prostaglandin E2 (PGE2) and prolactin. This effect was mediated by Smad and ERK activation. Addition of rosiglitazone, a PPAR gamma agonist, prevented TGF-β1 effect on endometrial cell proliferation. Furthermore, rosiglitazone inhibited TGF-β1 induced activation of ERK, consequently reducing PGE2 and prolactin production. CONCLUSION: TGF-β1-induced decidualization of endometrial stromal cells through Smad and ERK phosphorylation. PPAR gamma acts as a negative regulator of human endometrial cell decidualization in vitro.","자궁내막 탈락막화는 수정란의 착상 및 임신의 유지에 중요한 자궁 내막의 분화과정으로 TGF-β1가 관여한다고 알려져 있다. 본 연구를 통해 TGF-β1에 의해 유도된 인간자궁내막의 탈락막화 과정에서 ERK와 PPARγ의 역할을 규명하고자 하였다. 자궁내막 기질세포는 DMEM/F12 (10% FBS, 1nM E2 and 100nM P4) 조건에서 배양하였다. 연구 목적에 따라 TGF-β1 (5 ng/ml), Rosiglitazone (50 nM)과 PD98059 (20 μM)를 배양액에 첨가하였다. Trypan-Blue와 hemocytometer를 이용하여 현미경하에서 세포의 개수를 측정하였다. Enzyme-linked immunosorbent assay (ELISA)와 Western blotting 방법을 사용하여 Prostaglandin E2 (PGE2) 및 prolactin 단백질의 발현 정도를 관찰하였다. 배양액에 TGF-β1을 첨가하여 세포의 증식정도를 측정한 결과 TGF-β1이 세포의 증식을 억제하는 것을 알 수 있었다. 또한 배양된 세포로부터 PGE2 및 prolactin의 발현을 유도하는 것을 알 수 있었고, 이러한 TGF-β1의 작용은 Smad 및 ERK의 활성화를 통하여 일어남을 알 수 있었다. PPARγ의 기질인 rosiglitazone을 배양액에 첨가한 결과 TGF-β1에 의한 세포 증식의 억제가 역전되는 것을 알 수 있었다. 뿐만 아니라, 세포 내 ERK의 활성 역시 억제 시켰으며 이 결과 PGE2 와 prolactin의 발현이 감소 되는 것을 관찰할 수 있었다. 따라서 본 연구를 통해 TGF-β1에 의한 자궁내막 기질세포의 탈락막화는 Smad와 ERK의 활성화를 통하여 이루어지며 이러한 과정은 PPARγ 에 의해 억제됨을 확인하였다.","\"Ⅰ. INTRODUCTION = 1 Ⅱ. MATERIALS AND METHODS = 4 A. MATERIALS = 4 1. Cinical subjects and endometrial biopsies = 4 2. Reagents and antibodies = 4 B. METHODS = 5 1. Endometrial stromal cell isolation and primary cell culture = 5 2. Cell count by using trypan-blue dye = 6 3. Western blot analysis of prolactin, pSmad2/3, PPARγ, COX-2 and pEPK = 6 4. Measurement of Prostaglandin E₂ concentrations in the conditioned media = 7 5. Statistical analysis = 7 Ⅲ. RESULTS = 8 Ⅳ. DISCUSSION = 14 Ⅴ. CONCLUSION = 17 REFERENCES = 18 국문요약 = 24\"","Doctor"]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Role of Extracellular Signal­-Regulated Kinase and Peroxisome Proliferator-­Activated Receptor gamma on Transforming Growth Factor-­β1-­Induced Human Endometrial Stromal Cell Decidualization","Transforming Growth Factor-­β1에 의해 유도된 인간 자궁내막 기질세포의 탈락막화에서 Extracellular Signal-Regulated Kinase와 Peroxisome Proliferator-Activated Receptorγ 의 역할"]}]}],"canonical_facts":{"dc:contributor":["황, 경주","대학원 의학과","103765","장, 혜진"],"dc:creator":["장, 혜진"],"dc:date":["2011-01-26T05:22:12Z","2007"],"dc:description":["OBJECTIVE: To investigate the role of ERK and PPAR gamma on TGF-β1-induced human endometrial stromal cell decidualization in vitro. MATERIALS AND METHODS: Human endometrial tissues obtained by hysterectomy specimens from patients with conditions other than endometrial diseases such as leiomyoma. Endometrial stromal cells were cultured under the following conditions: DMEM/F-12 (10% FBS, 1 nM E2 and 100 nM P4). 5 ng/ml of TGF-β1, 50 nM of rosiglitazone (PPAR gamma agonist), and 20 μM of PD98059 (ERK inhibitor) were added according to experimental purposes. Trypan-blue and a hemocytometer were utilized to count the viable cell number. Enzyme-linked immunosorbent assay (ELISA) and Western blotting was employed to detect proteins. RESULTS: TGF-β1 inhibited proliferation of cultured human endometrial stromal cells and induced expression of prostaglandin E2 (PGE2) and prolactin. This effect was mediated by Smad and ERK activation. Addition of rosiglitazone, a PPAR gamma agonist, prevented TGF-β1 effect on endometrial cell proliferation. Furthermore, rosiglitazone inhibited TGF-β1 induced activation of ERK, consequently reducing PGE2 and prolactin production. CONCLUSION: TGF-β1-induced decidualization of endometrial stromal cells through Smad and ERK phosphorylation. PPAR gamma acts as a negative regulator of human endometrial cell decidualization in vitro.","자궁내막 탈락막화는 수정란의 착상 및 임신의 유지에 중요한 자궁 내막의 분화과정으로 TGF-β1가 관여한다고 알려져 있다. 본 연구를 통해 TGF-β1에 의해 유도된 인간자궁내막의 탈락막화 과정에서 ERK와 PPARγ의 역할을 규명하고자 하였다. 자궁내막 기질세포는 DMEM/F12 (10% FBS, 1nM E2 and 100nM P4) 조건에서 배양하였다. 연구 목적에 따라 TGF-β1 (5 ng/ml), Rosiglitazone (50 nM)과 PD98059 (20 μM)를 배양액에 첨가하였다. Trypan-Blue와 hemocytometer를 이용하여 현미경하에서 세포의 개수를 측정하였다. Enzyme-linked immunosorbent assay (ELISA)와 Western blotting 방법을 사용하여 Prostaglandin E2 (PGE2) 및 prolactin 단백질의 발현 정도를 관찰하였다. 배양액에 TGF-β1을 첨가하여 세포의 증식정도를 측정한 결과 TGF-β1이 세포의 증식을 억제하는 것을 알 수 있었다. 또한 배양된 세포로부터 PGE2 및 prolactin의 발현을 유도하는 것을 알 수 있었고, 이러한 TGF-β1의 작용은 Smad 및 ERK의 활성화를 통하여 일어남을 알 수 있었다. PPARγ의 기질인 rosiglitazone을 배양액에 첨가한 결과 TGF-β1에 의한 세포 증식의 억제가 역전되는 것을 알 수 있었다. 뿐만 아니라, 세포 내 ERK의 활성 역시 억제 시켰으며 이 결과 PGE2 와 prolactin의 발현이 감소 되는 것을 관찰할 수 있었다. 따라서 본 연구를 통해 TGF-β1에 의한 자궁내막 기질세포의 탈락막화는 Smad와 ERK의 활성화를 통하여 이루어지며 이러한 과정은 PPARγ 에 의해 억제됨을 확인하였다.","\"Ⅰ. INTRODUCTION = 1 Ⅱ. MATERIALS AND METHODS = 4 A. MATERIALS = 4 1. Cinical subjects and endometrial biopsies = 4 2. Reagents and antibodies = 4 B. METHODS = 5 1. Endometrial stromal cell isolation and primary cell culture = 5 2. Cell count by using trypan-blue dye = 6 3. Western blot analysis of prolactin, pSmad2/3, PPARγ, COX-2 and pEPK = 6 4. Measurement of Prostaglandin E₂ concentrations in the conditioned media = 7 5. Statistical analysis = 7 Ⅲ. RESULTS = 8 Ⅳ. DISCUSSION = 14 Ⅴ. CONCLUSION = 17 REFERENCES = 18 국문요약 = 24\"","Doctor"],"dc:format":["application/pdf"],"dc:identifier":["http://repository.ajou.ac.kr/handle/201003/1295","http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000002027","000000002027"],"dc:language":["en"],"dc:subject":["Decidualization","TGF-β1","PPAR gamma","자궁내막","탈락막화"],"dc:title":["Role of Extracellular Signal­-Regulated Kinase and Peroxisome Proliferator-­Activated Receptor gamma on Transforming Growth Factor-­β1-­Induced Human Endometrial Stromal Cell Decidualization","Transforming Growth Factor-­β1에 의해 유도된 인간 자궁내막 기질세포의 탈락막화에서 Extracellular Signal-Regulated Kinase와 Peroxisome Proliferator-Activated Receptorγ 의 역할"],"dc:type":["Thesis","Theses"]},"updated_at":"2026-07-24T00:51:19Z"}