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  1. Article: New Endothelial Mechanisms in Glomerular (Patho)biology and Proteinuria Development Captured by Intravital Multiphoton Imaging.

    Gyarmati, Georgina / Jacob, Chaim O / Peti-Peterdi, János

    Frontiers in medicine

    2021  Volume 8, Page(s) 765356

    Abstract: In the past two decades, intravital imaging using multiphoton microscopy has provided numerous new visual and mechanistic insights into glomerular biology and disease processes including the function of glomerular endothelial cells (GEnC), podocytes, and ...

    Abstract In the past two decades, intravital imaging using multiphoton microscopy has provided numerous new visual and mechanistic insights into glomerular biology and disease processes including the function of glomerular endothelial cells (GEnC), podocytes, and the development of proteinuria. Although glomerular endothelial injury is known to precede podocyte damage in several renal diseases, the primary role of GEnCs in proteinuria development received much less attention compared to the vast field of podocyte pathobiology. Consequently, our knowledge of GEnC mechanisms in glomerular diseases is still emerging. This review highlights new visual clues on molecular and cellular mechanisms of GEnCs and their crosstalk with podocytes and immune cells that were acquired recently by the application of multiphoton imaging of the intact glomerular microenvironment in various proteinuric disease models. New mechanisms of glomerular tissue remodeling and regeneration are discussed based on results of tracking the fate and function of individual GEnCs using serial intravital multiphoton imaging over several days and weeks. The three main topics of this review include (i) the role of endothelial injury and microthrombi in podocyte detachment and albumin leakage via hemodynamic and mechanical forces, (ii) the alterations of the endothelial surface layer (glycocalyx) and its interactions with circulating immune cells in lupus nephritis, and (iii) the structural and functional remodeling and regeneration of GEnCs in hypertension, diabetes, and other experimental injury conditions. By the comprehensive visual portrayal of GEnCs and the many other contributing glomerular cell types, this review emphasizes the complexity of pathogenic mechanisms that result in proteinuria development.
    Language English
    Publishing date 2021-10-13
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2021.765356
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  2. Article ; Online: A practical new way to measure kidney fibrosis.

    Peti-Peterdi, János

    Kidney international

    2016  Volume 90, Issue 5, Page(s) 941–942

    Abstract: Proper histological measurement of kidney fibrosis is essentially important in both clinical pathology and basic research using animal models of chronic kidney disease (CKD). However, standard histology techniques and their blind evaluation are ... ...

    Abstract Proper histological measurement of kidney fibrosis is essentially important in both clinical pathology and basic research using animal models of chronic kidney disease (CKD). However, standard histology techniques and their blind evaluation are cumbersome. Ranjit et al. applied an advanced optical microscopy technique for hassle-free, unbiased, and highly sensitive characterization of kidney fibrosis and tested it in a classic model of chronic kidney disease in mice. This commentary emphasizes the advantages and future promise of this new approach.
    Language English
    Publishing date 2016-10-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2016.07.036
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  3. Article ; Online: In vivo microscopy.

    Peti-Peterdi, János

    Nephrologie & therapeutique

    2016  Volume 12 Suppl 1, Page(s) S21–4

    Abstract: This article summarizes the past, present, and future promise of multiphoton excitation fluorescence microscopy for intravital kidney imaging. During the past 15years, several high-power visual research approaches have been developed using multiphoton ... ...

    Abstract This article summarizes the past, present, and future promise of multiphoton excitation fluorescence microscopy for intravital kidney imaging. During the past 15years, several high-power visual research approaches have been developed using multiphoton imaging to study the normal functions of the healthy, intact, living kidney, and the various molecular and cellular mechanisms of the development of kidney diseases. In this review, the main focus will be on intravital multiphoton imaging of the glomerulus, the structure and function of the glomerular filtration barrier, especially the podocyte. Examples will be given for the combination of two powerful research tools, in vivo multiphoton imaging and mouse genetics using commercially available whole animal models for the detailed characterization of glomerular cell types, their function and fate, and for the better understanding of the molecular mechanisms of glomerular pathologies. One of the new modalities of multiphoton imaging, serial imaging of the same glomerulus in the same animal over several days will be emphasized for its potential for further advancing the field of nephrology research.
    Language English
    Publishing date 2016-04
    Publishing country France
    Document type Journal Article
    ZDB-ID 2229575-6
    ISSN 1872-9177 ; 1769-7255
    ISSN (online) 1872-9177
    ISSN 1769-7255
    DOI 10.1016/j.nephro.2016.01.004
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  4. Article ; Online: Newly stemming functions of macula densa-derived prostanoids.

    Peti-Peterdi, János

    Hypertension (Dallas, Tex. : 1979)

    2015  Volume 65, Issue 5, Page(s) 987–988

    MeSH term(s) Animals ; Dinoprostone/genetics ; Gene Expression Regulation ; Hypertension/diet therapy ; Male ; Mesenchymal Stem Cells/physiology ; RNA, Messenger/genetics ; Receptors, Prostaglandin E, EP4 Subtype/genetics
    Chemical Substances RNA, Messenger ; Receptors, Prostaglandin E, EP4 Subtype ; Dinoprostone (K7Q1JQR04M)
    Language English
    Publishing date 2015-03-16
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.115.04739
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  5. Article ; Online: Physiological Mechanisms of Dietary Salt Sensing in the Brain, Kidney, and Gastrointestinal Tract.

    Stocker, Sean D / Kinsman, Brian J / Farquhar, William B / Gyarmati, Georgina / Peti-Peterdi, Janos / Sved, Alan F

    Hypertension (Dallas, Tex. : 1979)

    2023  Volume 81, Issue 3, Page(s) 447–455

    Abstract: Excess dietary salt (NaCl) intake is strongly correlated with cardiovascular disease and is a major contributing factor to the pathogenesis of hypertension. NaCl-sensitive hypertension is a multisystem disorder that involves renal dysfunction, vascular ... ...

    Abstract Excess dietary salt (NaCl) intake is strongly correlated with cardiovascular disease and is a major contributing factor to the pathogenesis of hypertension. NaCl-sensitive hypertension is a multisystem disorder that involves renal dysfunction, vascular abnormalities, and neurogenically-mediated increases in peripheral resistance. Despite a major research focus on organ systems and these effector mechanisms causing NaCl-induced increases in arterial blood pressure, relatively less research has been directed at elucidating how NaCl is sensed by various tissues to elicit these downstream effects. The purpose of this review is to discuss how the brain, kidney, and gastrointestinal tract sense NaCl including key cell types, the role of NaCl versus osmolality, and the underlying molecular and electrochemical mechanisms.
    MeSH term(s) Humans ; Sodium Chloride, Dietary/metabolism ; Sodium Chloride/metabolism ; Blood Pressure ; Kidney/metabolism ; Hypertension ; Brain/metabolism
    Chemical Substances Sodium Chloride, Dietary ; Sodium Chloride (451W47IQ8X)
    Language English
    Publishing date 2023-09-06
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.123.19488
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Mitochondrial TCA cycle intermediates regulate body fluid and acid-base balance.

    Peti-Peterdi, János

    The Journal of clinical investigation

    2013  Volume 123, Issue 7, Page(s) 2788–2790

    Abstract: Intrarenal control mechanisms play an important role in the maintenance of body fluid and electrolyte balance and pH homeostasis. Recent discoveries of new ion transport and regulatory pathways in the distal nephron and collecting duct system have helped ...

    Abstract Intrarenal control mechanisms play an important role in the maintenance of body fluid and electrolyte balance and pH homeostasis. Recent discoveries of new ion transport and regulatory pathways in the distal nephron and collecting duct system have helped to better our understanding of these critical kidney functions and identified new potential therapeutic targets and approaches. In this issue of the JCI, Tokonami et al. report on the function of an exciting new paracrine mediator, the mitochondrial the citric acid(TCA) cycle intermediate α-ketoglutarate (αKG), which via its OXGR1 receptor plays an unexpected, nontraditional role in the adaptive regulation of renal HCO(3⁻) secretion and salt reabsorption.
    MeSH term(s) Acid-Base Equilibrium ; Animals ; Ketoglutaric Acids/urine ; Kidney Tubules, Collecting/physiology ; Male ; Paracrine Communication
    Chemical Substances Ketoglutaric Acids
    Language English
    Publishing date 2013-06-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI68095
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  7. Article ; Online: A new view of macula densa cell protein synthesis.

    Shroff, Urvi Nikhil / Gyarmati, Georgina / Izuhara, Audrey / Deepak, Sachin / Peti-Peterdi, János

    American journal of physiology. Renal physiology

    2021  Volume 321, Issue 6, Page(s) F689–F704

    Abstract: Macula densa (MD) cells, a chief sensory cell type in the nephron, are endowed with unique microanatomic features including a high density of protein synthetic organelles and secretory vesicles in basal cell processes ("maculapodia") that suggest a so ... ...

    Abstract Macula densa (MD) cells, a chief sensory cell type in the nephron, are endowed with unique microanatomic features including a high density of protein synthetic organelles and secretory vesicles in basal cell processes ("maculapodia") that suggest a so far unknown high rate of MD protein synthesis. This study aimed to explore the rate and regulation of MD protein synthesis and their effects on glomerular function using novel transgenic mouse models, newly established fluorescence cell biology techniques, and intravital microscopy. Sox2-tdTomato kidney tissue sections and an
    MeSH term(s) Animals ; Autocrine Communication ; Diet, Sodium-Restricted ; Glomerular Filtration Rate ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Humans ; Intravital Microscopy ; Juxtaglomerular Apparatus/cytology ; Juxtaglomerular Apparatus/metabolism ; Luminescent Proteins/genetics ; Luminescent Proteins/metabolism ; Mice, Inbred C57BL ; Mice, Transgenic ; Microscopy, Fluorescence, Multiphoton ; Nitric Oxide Synthase Type I/genetics ; Nitric Oxide Synthase Type I/metabolism ; Paracrine Communication ; Protein Biosynthesis ; Renin/metabolism ; Signal Transduction ; Sodium, Dietary/metabolism ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism ; Tuberous Sclerosis Complex 2 Protein/genetics ; Tuberous Sclerosis Complex 2 Protein/metabolism ; Red Fluorescent Protein ; Mice
    Chemical Substances Luminescent Proteins ; Sodium, Dietary ; Tsc2 protein, mouse ; Tuberous Sclerosis Complex 2 Protein ; enhanced green fluorescent protein ; Green Fluorescent Proteins (147336-22-9) ; Nitric Oxide Synthase Type I (EC 1.14.13.39) ; Nos1 protein, mouse (EC 1.14.13.39) ; mTOR protein, mouse (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Renin (EC 3.4.23.15)
    Language English
    Publishing date 2021-10-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Video-Audio Media
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00222.2021
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    Uc I Zs.89: Show issues Location:
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  8. Article ; Online: Correction to: Long-Term Cell Fate Tracking of Individual Renal Cells Using Serial Intravital Microscopy.

    Schiessl, Ina Maria / Fremter, Katharina / Burford, James L / Castrop, Hayo / Peti-Peterdi, Janos

    Methods in molecular biology (Clifton, N.J.)

    2020  Volume 2150, Page(s) 243

    Abstract: The original version of this chapter was inadvertently published without a proper acknowledgement. The authors informed to insert the following acknowledgement in this chapter. ...

    Abstract The original version of this chapter was inadvertently published without a proper acknowledgement. The authors informed to insert the following acknowledgement in this chapter.
    Language English
    Publishing date 2020-02-19
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/7651_2019_278
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  9. Article ; Online: High glucose and renin release: the role of succinate and GPR91.

    Peti-Peterdi, János

    Kidney international

    2010  Volume 78, Issue 12, Page(s) 1214–1217

    Abstract: Diabetes mellitus is the most common and rapidly growing cause of end-stage renal disease. A classic hallmark of diabetes pathology is the activation of the intrarenal renin-angiotensin system (RAS), which may lead to hypertension and renal tissue injury, ...

    Abstract Diabetes mellitus is the most common and rapidly growing cause of end-stage renal disease. A classic hallmark of diabetes pathology is the activation of the intrarenal renin-angiotensin system (RAS), which may lead to hypertension and renal tissue injury, but the mechanism of RAS activation has been elusive. Recently, we described the intrarenal localization of the novel metabolic receptor GPR91 and established some of its functions in diabetes. These include the triggering of renin release in early diabetes via both vascular (endothelial) and tubular (macula densa) sites in the juxtaglomerular apparatus as well as the activation of MAP kinases in the distal nephron-collecting duct, which are important signaling mechanisms in diabetic nephropathy (DN) and renal fibrosis. GPR91 is a cell surface receptor for succinate and during the past few years it has provided a new paradigm for the mechanism of cell stress response in many organs. Beyond its traditional role in the tricarboxylic acid cycle, succinate now has an unexpected hormone-like signaling function, which may provide a feedback between local tissue metabolism, mitochondrial stress, and organ functions. Succinate accumulation in the local tissue environment and GPR91 signaling appear to be important early mechanisms by which cells detect and respond to hyperglycemia and trigger tissue injury in DN. Also, the distal nephron-collecting duct system, which is the major source of (pro)renin in diabetes and has the highest level of GPR91 expression in the kidney, may have an important, active, and early role in the pathogenesis of DN in contrast to the existing glomerulus-centric paradigm.
    MeSH term(s) Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/physiopathology ; Glomerular Filtration Rate/physiology ; Humans ; Hyperglycemia/metabolism ; Hyperglycemia/physiopathology ; Kidney Tubules, Distal/physiopathology ; Receptors, G-Protein-Coupled/physiology ; Renin/metabolism ; Signal Transduction/physiology ; Succinic Acid/metabolism
    Chemical Substances Receptors, G-Protein-Coupled ; SUCNR1 protein, human ; Succinic Acid (AB6MNQ6J6L) ; Renin (EC 3.4.23.15)
    Language English
    Publishing date 2010-09-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1038/ki.2010.333
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    Zs.A 797: Show issues Location:
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  10. Article: The role of TRPC6 calcium channels and P2 purinergic receptors in podocyte mechanical and metabolic sensing.

    Gyarmati, Georgina / Toma, Ildikó / Izuhara, Audrey / Burford, James L / Shroff, Urvi Nikhil / Papadouri, Stella / Deepak, Sachin / Peti-Peterdi, János

    Physiology international

    2021  

    Abstract: Podocyte calcium (Ca2+) signaling plays important roles in the (patho)physiology of the glomerular filtration barrier. Overactivation of podocyte transient receptor potential canonical (TRPC) channels including TRPC6 and purinergic signaling via P2 ... ...

    Abstract Podocyte calcium (Ca2+) signaling plays important roles in the (patho)physiology of the glomerular filtration barrier. Overactivation of podocyte transient receptor potential canonical (TRPC) channels including TRPC6 and purinergic signaling via P2 receptors that are known mechanosensors can increase podocyte intracellular Ca2+ levels ([Ca2+]i) and cause cell injury, proteinuria and glomerular disease including in diabetes. However, important mechanistic details of the trigger and activation of these pathways in vivo in the intact glomerular environment are lacking. Here we show direct visual evidence that podocytes can sense mechanical overload (increased glomerular capillary pressure) and metabolic alterations (increased plasma glucose) via TRPC6 and purinergic receptors including P2Y2. Multiphoton microscopy of podocyte [Ca2+]i was performed in vivo using wild-type and TRPC6 or P2Y2 knockout (KO) mice expressing the calcium reporter GCaMP3/5 only in podocytes and in vitro using freshly dissected microperfused glomeruli. Single-nephron intra-glomerular capillary pressure elevations induced by obstructing the efferent arteriole lumen with laser-induced microthrombus in vivo and by a micropipette in vitro triggered >2-fold increases in podocyte [Ca2+]i. These responses were blocked in TRPC6 and P2Y2 KO mice. Acute elevations of plasma glucose caused >4-fold increases in podocyte [Ca2+]i that were abolished by pharmacological inhibition of TRPC6 or P2 receptors using SAR7334 or suramin treatment, respectively. This study established the role of Ca2+ signaling via TRPC6 channels and P2 receptors in mechanical and metabolic sensing of podocytes in vivo, which are promising therapeutic targets in conditions with high intra-glomerular capillary pressure and plasma glucose, such as diabetic and hypertensive nephropathy.
    Language English
    Publishing date 2021-12-16
    Publishing country Hungary
    Document type Journal Article
    ZDB-ID 2896288-6
    ISSN 2498-602X
    ISSN 2498-602X
    DOI 10.1556/2060.2021.00205
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