Activation of Calcium Signaling in Isolated Rat Hepatocytes Is Accompanied by Shape Changes of Microvilli

Lange, Julia; Schlieps, Karsten; Lange, Klaus; Knoll-Köhler, E

doi:10.1006/excr.1997.3652

Cited by 24 publications

(31 citation statements)

References 31 publications

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“…Scanning electron microscopy (SEM) reveals that the small and regularly-formed microvilli of the unstimulated hepatocyte surface are rapidly transformed by vasopressin into large irregular protrusions. As shown by additional experiments, the loss of the normal shape of microvilli is always correlated with activation of Ca ϩϩ influx regardless of the way by which this activation was caused (Lange et al, 1997). Receptor-mediated activation of the PLC/ Ca ϩϩ signal pathway acts on the microvillar structure via depolymerization/reorganization of the microfilament bundle.…”

Section: Morphological Correlate Of the Activated Camentioning

confidence: 93%

“…This morphological correlate of the activated microvillar influx systems has been demonstrated for different cell types including C6 glioma cells (Lange et al, 1989), 3T3-L1 adipocytes (Lange et al, 1990), HIT cells (Lange and Brandt, 1993a), and isolated rat hepatocytes (Lange et al, 1997).…”

Section: Morphological Correlate Of the Activated Camentioning

confidence: 95%

“…Receptor-mediated activation of the PLC/ Ca ϩϩ signal pathway acts on the microvillar structure via depolymerization/reorganization of the microfilament bundle. Mechanical stress , action of proteases on the cell surface (Lange et al, 1997), thap- sigargin-induced store depletion (Lange et al, 1997), and alteration of membrane properties by lipophilic chemicals also accelerate Ca ϩϩ influx into the cell. The actions of all these effectors are accompanied by essentially the same type of shape changes of microvilli (Gartzke et al, 1997).…”

Section: Morphological Correlate Of the Activated Camentioning

confidence: 99%

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Microvillar Ca++ signaling: A new view of an old problem

Lange¹

1999

J. Cell. Physiol.

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Proceeding from the recent finding that the main components of the Ca++ signal pathway are located in small membrane protrusions on the surface of differentiated cells, called microvilli, a novel concept of cellular Ca++ signaling was developed. The main features of this concept can be summarized as follows: Microvilli are formed on the cell surface of differentiating or resting cells from exocytic membrane domains, growing out from the cell surface by elongation of an internal bundle of actin filaments. The microvillar tip membranes contain all functional important proteins synthesized such as ion channels and transporters for energy-providing substrates and structural components, which are, in rapidly growing undifferentiated cells, distributed over the whole cell surface by lateral diffusion. The microvillar shaft structure, a bundle of actin filaments, forms a dense cytoskeletal matrix tightly covered by the microvillar lipid membrane and represents an effective diffusion barrier separating the microvillar tip compartment (entrance compartment) from the cytoplasm. This diffusion barrier prevents the passage of low molecular components such as Ca++ glucose and other relevant substrates from the entrance compartment into the cytoplasm. The effectiveness of the actin-based diffusion barrier is modulated by various signal pathways and effectors, most importantly, by the actin-depolymerizing/reorganizing activity of the phospholipase C (PLC)-coupled Ca++ signaling. Moreover, the microvillar bundle of actin filaments plays a dual role in Ca++ signaling. It combines the function of a diffusion barrier, preventing Ca++ influx into the resting cell, with that of a high-affinity, ATP-dependent, and IP3-sensitive Ca++ store. Activation of Ca++ signaling via PLC-coupled receptors simultaneously empties Ca++ stores and activates the influx of external Ca++. The presented concept of Ca++ signaling is compatible with all established data on Ca++ signaling. Properties of Ca++ signaling, that could not be reconciled with the basic principles of the current hypothesis, are intrinsic properties of the new concept. Quantal Ca++ release, Ca(++)-induced Ca++ release (CICR), the coupling phenomen between the filling state of the Ca++ store and the activity of the Ca++ influx pathway, as well as the various yet unexplained complex kinetics of Ca++ uptake and release can be explained on a common mechanistic basis.

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Section: Morphological Correlate Of the Activated Camentioning

confidence: 93%

Section: Morphological Correlate Of the Activated Camentioning

confidence: 95%

Section: Morphological Correlate Of the Activated Camentioning

confidence: 99%

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Microvillar Ca++ signaling: A new view of an old problem

Lange¹

1999

J. Cell. Physiol.

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“…Because of tighter binding of divalent cations to fixed charge centers, divalent cation conduction is more restricted. increases following receptor-mediated disorganization of the microvillar bundle structure (40,43,44).…”

Section: The F-actin Diffusion Barrier Is a Cation Exchangermentioning

confidence: 99%

Cellular target of weak magnetic fields: ionic conduction along actin filaments of microvilli

Gartzke

Lange²

2002

American Journal of Physiology-Cell Physiology

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102

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Gartzke, Joachim, and Klaus Lange. Cellular target of weak magnetic fields: ionic conduction along actin filaments of microvilli. Am J Physiol Cell Physiol 283: C1333-C1346, 2002; 10.1152/ajpcell. 00167.2002.-The interaction of weak electromagnetic fields (EMF) with living cells is a most important but still unresolved biophysical problem. For this interaction, thermal and other types of noise appear to cause severe restrictions in the action of weak signals on relevant components of the cell. A recently presented general concept of regulation of ion and substrate pathways through microvilli provides a possible theoretical basis for the comprehension of physiological effects of even extremely low magnetic fields. The actin-based core of microfilaments in microvilli is proposed to represent a cellular interaction site for magnetic fields. Both the central role of F-actin in Ca 2ϩ signaling and its polyelectrolyte nature eliciting specific ion conduction properties render the microvillar actin filament bundle an ideal interaction site for magnetic and electric fields. Ion channels at the tip of microvilli are connected with the cytoplasm by a bundle of microfilaments forming a diffusion barrier system. Because of its polyelectrolyte nature, the microfilament core of microvilli allows Ca 2ϩ entry into the cytoplasm via nonlinear cable-like cation conduction through arrays of condensed ion clouds. The interaction of ion clouds with periodically applied EMFs and field-induced cation pumping through the cascade of potential barriers on the F-actin polyelectrolyte follows well-known physical principles of ion-magnetic field (MF) interaction and signal discrimination as described by the stochastic resonance and Brownian motor hypotheses. The proposed interaction mechanism is in accord with our present knowledge about Ca 2ϩ signaling as the biological main target of MFs and the postulated extreme sensitivity for coherent excitation by very low field energies within specific amplitude and frequency windows. Microvillar F-actin bundles shielded by a lipid membrane appear to function like electronic integration devices for signal-tonoise enhancement; the influence of coherent signals on cation transduction is amplified, whereas that of random noise is reduced. calcium signaling; cell differentiation; Brownian motor hypothesis; cyclotron resonance; hair cell; mechanoelectrical coupling; physiological effects MORE THAN A DECADE OF RESEARCH on field effects in biological systems has yielded rather compelling data for the involvement of the Ca 2ϩ signaling pathway as a primary and main target of magnetic fields (MFs). As first demonstrated by Liburdy and colleagues (52,53) and later on by a number of other authors, the Ca 2ϩ influx pathways of isolated or cultured cells are severely affected by rather low MF energies.The physiological relevance of this finding is high, because Ca 2ϩ represents the most important intracellular signal governing almost all physiological functions in differentiated cells. Most importantly, cytopla...

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“…This concept is further strengthened by the discovery of specific morphological changes of the cell surface characteristic for the stimulated Ca-signaling pathway (Lange and Brandt, 1993a;Lange et al, 1997Lange et al, , 1998.…”

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confidence: 96%

F‐actin‐based Ca signaling—a critical comparison with the current concept of Ca signaling

Lange¹,

Gartzke²

2006

Journal Cellular Physiology

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A short comparative survey on the current idea of Ca signaling and the alternative concept of F-actin-based Ca signaling is given. The two hypotheses differ in one central aspect, the mechanism of Ca storage. The current theory rests on the assumption of Ca-accumulating endoplasmic/sarcoplasmic reticulum-derived vesicles equipped with an ATP-dependent Ca pump and IP3- or ryanodine-sensitive channel-receptors for Ca-release. The alternative hypothesis proceeds from the idea of Ca storage at the high-affinity binding sites of actin filaments. Cellular sites of F-actin-based Ca storage are microvilli and the submembrane cytoskeleton. Several specific features of Ca signaling such as store-channel coupling, quantal Ca release, spiking and oscillations, biphasic and "phasic" uptake kinetics, and Ca-induced Ca release (CICR), which are not adequately described by the current concept, are inherent properties of the F-actin system and its dynamic state of treadmilling.

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Activation of Calcium Signaling in Isolated Rat Hepatocytes Is Accompanied by Shape Changes of Microvilli

Cited by 24 publications

References 31 publications

Microvillar Ca++ signaling: A new view of an old problem

Microvillar Ca++ signaling: A new view of an old problem

Cellular target of weak magnetic fields: ionic conduction along actin filaments of microvilli

F‐actin‐based Ca signaling—a critical comparison with the current concept of Ca signaling

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