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Abstrak :
[ABSTRAK
Latar belakang: Prematuritas merupakan salah satu kelainan yang masih menjadi masalah global. Kejadian prematuritas tidak hanya terjadi di negara berkembang tetapi juga di negara maju. Beberapa kondisi ibu hamil dapat memicu keadaan hipoksia dalam rahim sehingga menyebabkan kelahiran prematur. Keadaan plasenta menggambarkan kesejahteraan janin intra uteri. Kondisi hipoksia seluler memicu ekspresi HIF-1α yang menjadi faktor transkripsi bagi CA9 sebagai penanda hipoksia. Penelitian ini bertujuan menganalisis pengaruh hipoksia terhadap plasenta prematur. Metode: Sampel menggunakan plasenta prematur yang hipoksia (H) dan nonhipoksia (N) sebagai kontrol. Parameter yang dinilai adalah struktur histologis plasenta (Hematoksilin-Eosin), regulator hipoksia HIF-1α (imunohistokimia), dan penanda hipoksia CA9 (ELISA). Hasil: Penilaian struktur histologis menunjukkan adanya perbedaan jumlah pembuluh darah fetus antara kedua kelompok secara bermakna, dimana pada kelompok hipoksia jumlah pembuluh darah fetus lebih banyak dibandingkan kelompok non-hipoksia. Distribusi intensitas ekspresi HIF-1α kedua kelompok juga berbeda bermakna. Rerata kadar CA9 kedua kelompok tidak berbeda bermakna, namun terdapat kecenderungan rerata kadar CA9 kelompok hipoksia lebih tinggi 28% dibandingkan yang non-hipoksia. Kesimpulan: Pengaruh hipoksia terhadap plasenta prematur pada tingkat molekuler berupa stabilitas protein HIF-1α yang menyebabkan peningkatan jumlah pembuluh darah fetus dan terjadi kecenderungan peningkatan sintesis protein CA9.

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ABSTRACT
Background: Prematurity is a disorder that is still a global problem. Incidence of prematurity is a problem in developing and also in developed countries. Certain condition accompanying pregnancies may trigger uterine hypoxia, causing premature birth. The placental condition is related with the intra-uterine fetal condition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead to stabilization of HIF-1α protein, a transcription factor of CA9. This study aimed to analyze the effect of hypoxia on the premature placenta. Methods: Samples from hypoxic premature placenta (H) and non-hypoxic premature placenta (N) were collected. Parameters assessed were histological structure of the placenta (Hematoxylin-Eosin), expression of HIF-1α (immunohistochemistry) and the level of CA9 (ELISA). Results: Assessment of histological structure showed the number of fetal blood vessels were differed significantly between the two group, wherein the hypoxia group was more than the non-hypoxia. The distributions of HIF-1α expression between the two groups were also differed significantly. The average level of CA9 between two groups were not significant, but there is a tendency of higher level of CA9 in the hypoxia group (28% higher compared to the non-hypoxia group). Conclusion: It is concluded that the effect of the hypoxia on premature placenta in this study occured at molecular level and lead to HIF-1α protein stability that causes an increase of the number of fetal blood vessel and synthesis of CA9 protein.;Background: Prematurity is a disorder that is still a global problem. Incidence of prematurity is a problem in developing and also in developed countries. Certain condition accompanying pregnancies may trigger uterine hypoxia, causing premature birth. The placental condition is related with the intra-uterine fetal condition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead to stabilization of HIF-1α protein, a transcription factor of CA9. This study aimed to analyze the effect of hypoxia on the premature placenta. Methods: Samples from hypoxic premature placenta (H) and non-hypoxic premature placenta (N) were collected. Parameters assessed were histological structure of the placenta (Hematoxylin-Eosin), expression of HIF-1α (immunohistochemistry) and the level of CA9 (ELISA). Results: Assessment of histological structure showed the number of fetal blood vessels were differed significantly between the two group, wherein the hypoxia group was more than the non-hypoxia. The distributions of HIF-1α expression between the two groups were also differed significantly. The average level of CA9 between two groups were not significant, but there is a tendency of higher level of CA9 in the hypoxia group (28% higher compared to the non-hypoxia group). Conclusion: It is concluded that the effect of the hypoxia on premature placenta in this study occured at molecular level and lead to HIF-1α protein stability that causes an increase of the number of fetal blood vessel and synthesis of CA9 protein., Background: Prematurity is a disorder that is still a global problem. Incidence of prematurity is a problem in developing and also in developed countries. Certain condition accompanying pregnancies may trigger uterine hypoxia, causing premature birth. The placental condition is related with the intra-uterine fetal condition. Cellular hypoxic condition caused by systemic chronic hypoxia, lead to stabilization of HIF-1α protein, a transcription factor of CA9. This study aimed to analyze the effect of hypoxia on the premature placenta. Methods: Samples from hypoxic premature placenta (H) and non-hypoxic premature placenta (N) were collected. Parameters assessed were histological structure of the placenta (Hematoxylin-Eosin), expression of HIF-1α (immunohistochemistry) and the level of CA9 (ELISA). Results: Assessment of histological structure showed the number of fetal blood vessels were differed significantly between the two group, wherein the hypoxia group was more than the non-hypoxia. The distributions of HIF-1α expression between the two groups were also differed significantly. The average level of CA9 between two groups were not significant, but there is a tendency of higher level of CA9 in the hypoxia group (28% higher compared to the non-hypoxia group). Conclusion: It is concluded that the effect of the hypoxia on premature placenta in this study occured at molecular level and lead to HIF-1α protein stability that causes an increase of the number of fetal blood vessel and synthesis of CA9 protein.]

Abstrak :
ABSTRAK Latar Belakang: Keadaan hipoksia akan menimbulkan respons adaptasi untuk mempertahankan homeostasis tubuh. Perubahan fisiologis (peningkatan denyut jantung, nadi, dan frekuensi pernafasan) terjadi untuk menjamin penyediaan oksigen terutama untuk otak. Faktor transkripsi HIF-1 yang penting untuk mengatasi hipoksia, terdiri atas dua subunit yaitu HIF-1α dan HIF-1β yang dalam keadaan hipoksia membentuk heterodimer dan mengatur ekspresi sejumlah gen target untuk mengatasi hipoksia. Hipoksia akan menyebabkan produksi H+ oleh sel meningkat. Paru akan mengurangi keadaan melalui eksresi CO2 dan H2O. Proses ini membutuhkan enzim anhidrase karbonat (CA). Peran EKA yang disintesis di paru diperlukan untuk menaikan tekanan darah. Tujuan: Penelitian ini bertujuan untuk mengetahui respons HIF-1α, CA dan EKA pada paru tikus yang mengalami hipoksia sistemik kronik. Metode: 25 ekor tikus jantan Sprague-Dawley dibagi secara acak dalam 5 kelompok dan 4 kelompok diinduksi hipoksia normobarik sistemik selama 1, 3. 5, dan 7 hari. Dilakukan pengukuran protein HIF-1α (ELISA), ekspresi relatif mRNA HIF-1α, CA9 dan Ace1 (real time RT-PCR satu langkah). Aktivitas enzim CA total dan aktivitas EKA total (metode spektrofotometri). Hasil: Ekspresi mRNA HIF-1α meningkat pada hari ke 5 induksi hipoksia (ANOVA, p=0,006), protein HIF-1α mengalami peningkatan hingga hari ke 7 hipoksia (ANOVA, p=0,038), dan keduanya berkorelasi sedang dan bermakna (Pearson, R=0,426). Ekspresi mRNA CA9 dan aktivitas CA total meningkat pada hipoksia (p>0,05), dan berkorelasi sedang. Ekspresi mRNA Ace1 meningkat seiring dengan lamanya induksi (p>0,05), sedangkan aktivitas EKA total meningkat pada hari ke 3 hipoksia, dan berkorelasi sangat lemah. Hasil uji korelasi juga menunjukkan hubungan yang kuat antara protein HIF-1α dengan ekspresi mRNA Ace1, namun sangat lemah dengan ekspresi mRNA CA9. Kesimpulan: Terjadi peningkatan HIF-1α, CA dan EKA selama induksi hipoksia pada paru tikus. Protein HIF-1α meregulasi ekspresi CA9 dan Ace1.

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ABSTRACT Background: Hypoxia will cause adaptation response to maintain the body homeostasis. Physiological changes (increased heart rate, pulse, and respiratory rates) occur to supply oxygen especially brain. The transcription factor HIF-1 is important to overcome hypoxia condition, which composed of two subunits: HIF-1α and HIF-1β to form a heterodimer, and then regulate the expression of a target gene. Hypoxia causes increase H+ production in the cells. Lungs will decrease this condition through CO2 and H2O excretion. This process requires the enzyme carbonic anhydrase (CA). The blood pressure increases during hypoxia and ACE which is synthesized in the lung required increasing the blood pressure through renin angiotensin system (RAS). Aims: To analyze response of HIF-1α, carbonic anhydrase, and angiotensin converting enzyme in the chronically hypoxia. Methods: The lung tissues of 25 young male Sprague-Dawley rats were exposed to chronic systemic hypoxia (O2 10%: N290%) for 1, 3, 5, and 7 days. mRNA expression of HIF-1α, CA9, and Ace1 (one step real time RT-PCR). HIF-1α protein was determined with ELISA. The activities of CA and ACE were measured spectrophotometrically. Results: mRNA expression of HIF-1α increased in 5 days after induction (ANOVA, p=0,006), and protein HIF-1α was found to be the highest at 7 days after induction (ANOVA, p=0,038), and both of them was correlated significant. The highest expression of CA9 and specific activities of total CA were measured in 5 days after induction (p<0,05). Expression of Ace1 increased during induction, but not the specific activities of ACE total. A Strong correlation was found between HIF-1α protein with Ace1 mRNA expression, but not with CA9 mRNA expression. Conclusions: During chronic hypoxia, an increase HIF-1α, CA and ACE. HIF-1α protein can regulate CA9, and Ace1 expression.